NSG-430 Exam 3

traction

-Traction is used to: (1) Prevent or reduce pain and muscle spasm (e.g., whiplash, unrepaired hip fracture) (2) Immobilize a joint or part of the body (3) Reduce a fracture or dislocation (4) Treat a pathologic joint condition (e.g., tumor, infection) -Traction devices apply a pulling force on a fractured extremity to attain realignment, while countertraction pulls in the opposite direction. -The two most common types of traction are skin traction and skeletal traction. Skin Traction: -Skin traction is generally used for short-term treatment (48 to 72 hours) until skeletal traction or surgery is possible. -Tape, boots, or splints are applied directly to the skin to maintain alignment, primarily to help diminish muscle spasms in the injured extremity. -The traction weights are usually limited to 5 to 10 lbs (2.3 to 4.5 kg). -A Buck's traction boot is a type of skin traction used preoperatively for the patient with a hip fracture to reduce muscle spasms Buck's traction is used to immobilize a fracture, prevent hip flexion contractures, and reduce muscle spasms. -In skin traction, regular assessment of the skin is a priority because pressure points and skin breakdown may develop quickly. -Assess key pressure points every 2 to 4 hours. Skeletal Traction: -Skeletal traction, generally in place for longer periods than skin traction, is used to align injured bones and joints or to treat joint contractures and congenital hip dysplasia. -It provides a long-term pull that keeps the injured bones and joints aligned. -To apply skeletal traction, the surgeon inserts a pin or wire into the bone, and weights are attached to align and immobilize the injured body part. -Weight for skeletal traction ranges from 5 to 45 lbs (2.3 to 20.4 kg). -The use of too much weight can result in delayed union or nonunion. -The major complications of skeletal traction are infection at the pin insertion site and the effects of prolonged immobility. -When traction is used to treat fractures, the forces are usually exerted on the distal fragment to obtain alignment with the proximal fragment. -One of the more common types of skeletal traction is balanced suspension traction -Fracture alignment depends on the correct positioning and alignment of the patient while the traction forces remain constant. -For extremity traction to be effective, forces must be pulling in the opposite direction (countertraction). -Countertraction is commonly supplied by the patient's body weight or by weights pulling in the opposite direction and may be augmented by elevating the end of the bed. -Traction must be maintained continuously. -Keep the weights off the floor and moving freely through the pulleys.

heat related trauma

-Brief exposure to intense heat or prolonged exposure to less intense heat leads to heat stress. -This occurs when thermoregulatory mechanisms such as sweating, vasodilation, and increased respirations cannot compensate for exposure to increased ambient temperatures. -Ambient temperature is a product of environmental temperature and humidity. -Strenuous activities in hot or humid environments, clothing that interferes with perspiration, high fevers, and preexisting illnesses predispose individuals to heat stress. Risk Factors: -Age: •Infants •Older adults -Environmental Conditions: •High environmental temperatures •High relative humidity -Preexisting Illness: •Cardiovascular disease •Cystic fibrosis •Dehydration •Diabetes mellitus •Obesity •Previous stroke or other central nervous system lesion •Skin disorders (e.g., large burn scars) -Prescription Drugs: •Anticholinergics •Antihistamines •Antiparkinsonian drugs •Antispasmodics •β-Adrenergic blockers •Butyrophenones •Diuretics •Phenothiazines •Tricyclic antidepressants -Alcohol -Street Drugs: •Amphetamines •Jimson weed •Lysergic acid diethylamide (LSD) •Phencyclidine (PCP) •3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy) Heat Exhaustion: -Caused by decreased fluid intake, increased heat exposure, and increased activity -Body temp above 38.8 degrees Celsius or 102 degrees Fahrenheit -Headache -Fatigue -Weakness -Skin moist/ sweating orthostatic -Decreased blood pressure: orthostatic -Increased pulse -Anxiety (confusion) -Management: salt and water replacement, rest Heat Stroke: -Anxiety (confusion) -Skin hot and dry -Na+ and K+ depletion -Impaired sweating -Listlessness -Increased body temperature (above 40.0 degrees Celsius or 105 degrees Fahrenheit) -Cerebral edema: seizures, delirium, coma -Increased pulse and heart rate -Hypotension -Management: cooling, rest, fluid and electrolyte support Nursing Interventions: -Give patients with heat stroke water and Gatorade to help rehydrate them -Heat exhaustion is more severe: can cause seizures, body temperature can be as high as 105 degrees, can lead to cerebral edema -Goals for heat exhaustion is to rehydrate patient and bring their temperature down - put cool wet sheet on patients' skin, put ice pack in their axillary or groin region; put wet washcloth on patients' forehead or back of their neck; put a fan in front of them

myofascial pain syndromes

-Chronic complex of syndromes: fibromyalgia, myalgia, and myositis -Myofascial pain syndrome is a chronic form of muscle pain. -It is marked by musculoskeletal pain and tenderness, typically in the chest, neck, shoulders, hips, and lower back. -Referred pain from these muscle groups can also travel to the buttocks, hands, and head, causing severe headaches. -Temporomandibular joint pain may also originate in myofascial pain. -Regions of pain are often within the connective tissue (fascia) that covers skeletal muscles. -Trigger or tender points are thought to activate a characteristic pattern of pain that can be worse with activity or stress. -Patients complain of deep, aching pain accompanied by a sensation of burning, stinging, and stiffness. Examples of this syndrome include fibromyalgia, myalgia, and myositis Treatment: -Physical therapy -"Spray and stretch" method: painful area is iced or sprayed with a coolant and then stretched -Topical patches -Trigger point injections -Massage, acupuncture, biofeedback, ultrasound

diffuse injury

-Concussion (a sudden transient mechanical head injury with disruption of neural activity and a change in the LOC) is considered a minor diffuse head injury. -The patient may or may not lose total consciousness with this injury. -Typical signs of concussion include a brief disruption in LOC, amnesia regarding the event (retrograde amnesia), and headache. The manifestations are generally of short duration. -If the patient has not lost consciousness, or if the loss of consciousness lasts less than 5 minutes, the patient is usually discharged from the care facility with instructions to notify the HCP if symptoms persist or if behavioral changes are noted. -Postconcussion syndrome may develop in some patients and is usually seen anywhere from 2 weeks to 2 months after the injury. -Manifestations include persistent headache, lethargy, personality and behavioral changes, shortened attention span, decreased short-term memory, and changes in intellectual ability. -This syndrome can significantly affect the patient's abilities to perform activities of daily living. -Although concussion is generally considered benign and usually resolves spontaneously, the signs and symptoms may be the beginning of a more serious, progressive problem, especially in a patient with a history of prior concussion or head injury. -At the time of discharge, it is important to give the patient and caregiver instructions for observation and accurate reporting of symptoms or changes in neurologic status. Diffuse Axonal Injury: -Diffuse axonal injury (DAI) is widespread axonal damage occurring after a mild, moderate, or severe TBI. -The damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus, and brainstem. -Initially, DAI was believed to occur from the tensile forces of trauma that sheared axons, resulting in axonal disconnection. -There is increasing evidence that axonal damage is not preceded by an immediate tearing of the axon from the traumatic impact, but rather the trauma changes the function of the axon, resulting in axon swelling and disconnection. -This process takes approximately 12 to 24 hours to develop and may persist longer. -The clinical signs of DAI are varied but may include a decreased LOC, increased ICP, decortication or decerebration, and global cerebral edema. -Approximately 90% of patients with DAI remain in a persistent vegetative state. -Patients with DAI who survive the initial event are rapidly triaged to an ICU where they will be vigilantly watched for signs of increased ICP and treated for increased ICP.

penetrating chest trauma injury

-Guns, knives -Worry about infection and how far the bullet fragments went into the body Pneumothorax: -Air collects in pleural space eventually collapsing the lung -Simple: collection of air -Open: air enters pleural space from a chest wound -Dyspnea, tachypnea -Decreased or absent breath sounds -Chest pain -Open sucking wound Tension Pneumothorax: -Life threatening -Lung collapses -Severe respiratory distress -Distended neck veins -Hypotension -Tracheal deviation -Cyanosis Hemothorax: -Blood collects in the pleural space -1500 ml+ -Chest pain -Signs of shock -Dyspnea, tachypnea -Dullness to percussion Cardiac Tamponade: -Blood collects in pericardial sac -Decreases cardiac output -Dyspnea -Cyanosis -Beck's Triad: distended neck veins, hypotension, muffled heart tones -Signs of shock Aortic Injury: -10-30% mortality -Ascending aorta injury is immediately fatal -Hypotension -Widened mediastinum -Loud systolic murmur -Chest pain -Decreased level of consciousness

anaphylactic shock

-Introduction of an antigen into a sensitive individual, initiating an antigen-antibody response -Release of vasoactive mediators and histamine -As antigens enter the body, antigens are produced that attach to mast cells and basophils. -Mast cells in the lungs, around blood vessels, in connective tissue, and in the uterus release vasoactive mediators in response to exposure to a common antigen that causes anaphylaxis. -Causes: severe allergic reaction Clinical Manifestations: -The clinical presentation of anaphylactic shock consists of upper and lower airway, angioedema, cardiovascular, and integumentary symptoms. -Angioedema symptoms consist of swelling of the lips, eyes, tongue, hands, feet, and genitalia. -Tachycardia and hypotension are the primary cardiovascular symptoms. -Cutaneous reactions that stimulate itching and pain lead to pruritus and urticaria. Treatment: -Management of an anaphylactic reaction involves removal of the offending agent and stabilization of the patient's airway. -The drug of choice for treating anaphylactic reactions is epinephrine, an adrenergic agent that promotes bronchodilation and vasoconstriction. -Histamine blocking agents such as ranitidine and diphenhydramine(Benadryl) are appropriate medications but are used as secondary agents. -Corticosteroids may be used to reduce inflammation. -Intravenous fluid therapy may be necessary to counteract hypotension (causes massive vasodilation)

viral meningitis

-Most common causes are enterovirus, arbovirus, HIV, and HSV -Most often spread through direct contact with respiratory secretions -Usually presents as headache, fever, photophobia, and stiff neck •Fever may be moderate or high -There are usually no symptoms of brain involvement. Diagnostic Testing: -The Xpert EV test is used to rapidly diagnose viral meningitis. -A sample of CSF is used to determine if enterovirus is present, and results are available within hours of symptom onset. -The CSF can be clear or cloudy, and the typical finding is lymphocytosis -Organisms are not seen on Gram stain or acid-fast smears. •Polymerase chain reaction (PCR) used to detect viral-specific deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) is a highly sensitive method for diagnosing CNS viral infections. Treatment: -Antibiotics are the best defense for bacterial meningitis and can be easily discontinued if the meningitis is found to be viral. -Treat with antibiotics after obtaining diagnostic sample but before receiving test results -Viral meningitis is managed symptomatically because the disease is self-limiting. -Full recovery from viral meningitis is expected. -Rare sequelae include persistent headaches, mild mental impairment, and incoordination.

inflammatory brain disorders

-Most common inflammatory conditions of the brain and spinal cord -Brain abscesses -Meningitis -Encephalitis: •10% to 30% mortality rate •Long-term neurologic deficits among survivors -Inflammation can be caused by bacteria, viruses, fungi, and chemicals (e.g., contrast media used in diagnostic tests, blood in the subarachnoid space). -CNS infections may occur via the bloodstream, by extension from a primary site, or along cranial and spinal nerves. -The mortality rate for inflammatory conditions of the brain is approximately 10% to 30% in the general population, with higher rates in older patients. -Up to 19% of those who recover can have long-term neurologic deficits, including hearing loss. -Staph and strep infections are common causes of inflammatory brain disorders -Mosquitoes spread encephalitis

snake bites (envenomation)

-People bitten by snakes go into DIC: clotting cascade is interrupted, they start bleeding and clotting at the same time -Coagulation abnormalities are due directly to snake venom interference with the coagulation cascade What to Do: -CroFab is a venom-specific fragment of IgG, which binds and neutralizes venom toxin, helping to remove the toxin from the target tissue and eliminate it from the body. -Anti venom -Need 3 vials, but is $3800 a vial -Keep them calm -Do not put a tourniquet or cold cloth on them -Also do not cut the site of the bite and/or suck venom out -Give them IV meds, give them pain medication, keep temperature not too hot and not too cold -Prognosis depends on whether the snake hit an artery or vein Prevention: -Don't reach into bushes, caves, or holes -If tubing in the river, do not go near the reeds -If hiking, wear boots and long pants

heat exhaustion

-Prolonged exposure to heat over hours or days -Clinical syndrome characterized by: •Fatigue •Nausea •Vomiting •Extreme thirst •Feelings of anxiety •Tachycardia •Dilated pupils •Mild confusion •Ashen color •Profuse diaphoresis •Hypotension and mild to severe temperature elevation (99.6º to 105.8º F [37.5º to 41º C]) due to dehydration -Heat exhaustion usually occurs in individuals engaged in strenuous activity in hot, humid weather, but it also occurs in sedentary individuals. Treatment: -Place patient in cool area and remove constrictive clothing -Monitor the patient for ABCs, including heart dysrhythmias (due to electrolyte imbalances). -Start oral fluid and electrolyte replacement unless the patient is nauseated. -Salt tablets are not used because of potential gastric irritation and hypernatremia. -Start a 0.9% normal saline IV solution if oral solutions are not tolerated. -An initial fluid bolus may be needed to correct hypotension. -However, correlate fluid replacement to clinical and laboratory findings. -Place a moist sheet over the patient to decrease core temperature through evaporative heat loss. -Consider hospital admission for the older adult, the chronically ill, or those who do not improve within 3 to 4 hours.

brain abscess

-Pus within brain tissue -Results from a local or systemic infection -Primary infective organisms: •Streptococci •Staphylococcus aureus -Direct extension from an ear, tooth, mastoid, or sinus infection is the primary cause. -Other causes for brain abscess formation include spread from a distant site (e.g., pulmonary infection, bacterial endocarditis), skull fracture, and prior brain trauma or surgery. -Vomiting is projectile Clinical Manifestations: -Similar to meningitis and encephalitis -Headache -Fever -Nausea and vomiting -Signs of increased ICP: •Drowsiness •Confusion •Seizures -Symptoms reflect local area of abscess -CT and MRI used to diagnose -Focal symptoms may be present and reflect the local area of the abscess. -For example, visual field defects or psychomotor seizures are common with a temporal lobe abscess, whereas an occipital abscess may be accompanied by visual impairment and hallucinations. Primary Treatment: -Antimicrobial therapy -Symptomatic treatment for other manifestations -Abscess may need to be drained or removed if drug therapy is not effective -Nursing measures are similar to those for management of meningitis or increased ICP. -If surgical drainage or removal is the treatment of choice, nursing care is similar to that described under cranial surgery.

human bites

-Result in puncture wounds or lacerations -High risk of infection: oral bacterial flora (Staph and Strep) -Risk for hepatitis virus -Risk for tissue damage -Human jaw has great crushing ability -Infection rates as high as 50% when treatment is not obtained within 24 hrs -Hands, fingers, ears, nose, vagina, and penis are the most common sites of human bites and are frequently a result of violence or sexual activity. -Patients with Boxer's fracture (fracture of the fourth or fifth metacarpal) often have concurrent open wounds on the knuckles from striking teeth. -The human jaw has great crushing ability, causing laceration, puncture, crush injury, soft tissue tearing, and even amputation. -Wounds over joints -Wounds > 6-12 hours old -Puncture wounds Bites on hand or foot Initial Treatment: -Clean with copious irrigation, debridement, tetanus prophylaxis, and analgesics -Prophylactic antibiotics for bites at risk for infection -Leave puncture wounds open; don't suture closed open or loose sutures due to infection/ abscesses. -Splint wounds over joints. -Lacerations are loosely sutured. -However, initial closure is used for facial wounds. -The patient is admitted for IV antibiotic therapy when an infection is present. -These patients have an increased incidence of cellulitis, osteomyelitis, and septic arthritis. -Report animal and human bites to the police as required. -People with vagina or penis bites often have trouble peeing: swelling makes it hard to void

facial fractures

-Traumatic injury: falls, MVA, sports (eye-globe rupture, orbital fracture (blow-out) -Airway maintenance, suctioning, positioning -Tracheostomy to by-pass obstruction -Facial and cervical injuries often occur together -Treat as cervical spine injury present until proven negative -Neuro assessment: GCS, LOC, EOMs, pupillary response, grips and pushes Types of Facial Fractures: -Frontal bone: rapid edema that may mask underlying fractures -Periorbital bone: possible frontal sinus involvement, entrapment of ocular muscles -Nasal bone: displacement of nasal bones, nosebleed (epistaxis) -Zygomatic arch: depression of cheek bone (zygomatic arch) and entrapment of ocular muscles -Maxilla: segmental motion (instability) of maxilla and tooth fracture at socket -Mandible: tooth fractures, bleeding, limited motion of mandible Immobilization: -Maxillary: more stable usually -Mandibular: unstable •Splinted to maxilla to stabilize •Intermaxillary fixation Postoperative Care: -Airway and nausea/vomiting management are priorities -Elevate HOB, turn to side to maintain airway -Oral hygiene -Communication -Pain management -Nutrition -Safety concerns at bedside •Scissors, wire cutters: remove if concerns with breathing or airway, provide home teaching •Emergency tracheostomy kit •Suction set up with Jonker tip •NG tube if persisting vomitus •Antiemetics •Method of communicating

venous thromboembolism (VTE)

-Veins of the lower extremities and pelvis are highly susceptible to thrombus formation after a fracture, especially a hip fracture. -Venous thromboembolism (VTE) may also occur after total hip or total knee replacement surgery. -In patients with limited mobility, venous stasis is aggravated by inactivity of muscles that normally assist in the pumping action of venous blood from the extremities to the heart. -Because of the high risk of VTE in the orthopedic surgical patient, prophylactic anticoagulant drugs such as (1) warfarin (Coumadin), (2) low-molecular-weight heparin (LMWH) (e.g., enoxaparin [Lovenox], fondaparinux [Arixtra], or rivaroxaban [Xarelto]) may be ordered. -In addition to wearing compression gradient stockings (antiembolism hose) and using sequential compression devices, the patient should dorsiflex and plantar flex the ankle of an affected lower extremity against resistance and perform ROM exercises on the unaffected leg.

frostbite

-Cold injuries may be localized (frostbite) or systemic (hypothermia). -Contributing factors include age, duration of exposure, environmental temperature, homelessness, preexisting conditions (e.g., diabetes mellitus, peripheral vascular disease), drugs that suppress shivering (e.g., opioids, psychotropic agents, antiemetics), and alcohol intoxication. -Alcohol causes peripheral vasodilation, increases sensation of warmth, and depresses shivering. -Smokers have an increased risk of cold-related injury because of the vasoconstrictive effects of nicotine. -Frostbite is true tissue freezing that results in the formation of ice crystals in the tissues and cells. -Peripheral vasoconstriction is the initial response to cold stress and results in a decrease in blood flow and vascular stasis. -As cellular temperature decreases and ice crystals form in intracellular spaces, the organelles are damaged and the cell membrane destroyed. -This results in edema. -Other factors that affect severity include skin color (dark-skinned people are more prone to frostbite), lack of acclimatization, previous episodes, exhaustion, ambient temperature, length of exposure, type and condition of clothing (wet/dry), contact with metal surfaces, and poor peripheral vascular status. -Superficial frostbite involves skin and subcutaneous tissue, usually the ears, nose, fingers, and toes. -The skin appearance ranges from waxy pale yellow to blue to mottled, and the skin feels crunchy and frozen. -The patient may complain of tingling, numbness, or a burning sensation. -Handle the area carefully and never squeeze, massage, or scrub the injured tissue because it is easily damaged. -Unless necessary, do not walk on feet or toes with frostbite -Do not use a fireplace, heat lamp, radiator, or stove for warming -Do not use a heating pad or electric blanket for warming -Remove clothing and jewelry because they may constrict the extremity and decrease circulation. -Superficial frostbite : immerse the affected area in circulating water that is temperature controlled (98.6° to 104° F) [37° to 40° C]). -Soak injured area until it flushes pink, keep water warm and fresh, keep injured area away from sides and bottom of the tub -Use warm soaks for the face. -The patient often experiences a warm, stinging sensation as tissue thaws. -Blisters form within a few hours. -The blisters should be debrided and a sterile dressing applied. -Avoid heavy blankets and clothing because friction and weight can lead to sloughing of damaged tissue. -Rewarming is extremely painful. -Residual pain may last weeks or even years. -Give analgesia and tetanus prophylaxis as appropriate. -Evaluate the patient with superficial frostbite for systemic hypothermia. -Warm water is very helpful: painful because nerves are reawakening, so premedicate them -Can also heat IV fluids Deep Frostbite: -Involves muscle, bone, and tendon -Skin is white, hard, insensitive to touch -Area has the appearance of deep thermal injury with mottling gradually progressing to gangrene -Immerse in a temperature controlled circulating water bath 98.6º to 104º F until flushing occurs distal to the injured area -Elevate to ↓ edema after rewarming -Significant edema within 3 hours -Blistering in 6 hours to days -IV analgesia -Tetanus prophylaxis -Evaluate for systemic hypothermia: •Hospitalization may be indicated •Amputation may be required

neurovascular nursing assessment

-Perform a focused physical assessment for the following clinical manifestations: -General: •Apprehension, guarding of injured site -Integumentary: •Skin lacerations, pallor and cool skin or bluish and warm skin distal to injury; ecchymosis, hematoma, edema at site of fracture -Cardiovascular: •Reduced or absent pulse distal to injury, ↓ skin temperature, delayed capillary refill -Neurovascular •Paresthesias, absent or ↓ sensation, hypersensation -Musculoskeletal: •Restricted or lost function of affected part; local bony deformities, abnormal angulation; shortening, rotation, or crepitation of affected part; muscle weakness -Possible Diagnostic Findings: •Identification and extent of fracture on x-ray, bone scan, CT scan, or MRI -Place special emphasis on the region distal to the site of injury. -Document clinical findings before fracture treatment is initiated to avoid doubts about whether a problem discovered later was missed during the original examination or was caused by the treatment. Neurovascular Assessment: -Musculoskeletal injuries have the potential for causing changes in the neurovascular status of an injured extremity. -Application of a cast or constrictive dressing, poor positioning, and physiologic responses to the traumatic injury can cause nerve or vascular damage, usually distal to the injury. -The neurovascular assessment should consist of peripheral vascular assessment (color, temperature, capillary refill, peripheral pulses, and edema) and a peripheral neurologic assessment (sensation, motor function, and pain). -Peripheral vascular assessment: •Assess an extremity's color (pink, pale, cyanotic) and temperature (hot, warm, cool, cold) in the area of the affected extremity. •Pallor or a cool/cold extremity below the injury could indicate arterial insufficiency. •A warm, cyanotic extremity could indicate poor venous return. •Assess capillary refill (blanching of the nail bed). A compressed nail bed should return to its original color is within 3 seconds. •Compare pulses on both the unaffected and injured extremity to identify differences in rate or quality. This contralateral evaluation is critical. Pulses are described as strong, diminished, audible by Doppler, or absent. •A diminished or absent pulse distal to the injury can indicate vascular dysfunction and insufficiency. •Also assess peripheral edema. Pitting edema may be present with severe injury. -Peripheral neurologic assessment: •Assess ulnar, median, and radial nerve function to evaluate sensation and motor innervation in the upper extremity. •Assess motor function by asking the patient to abduct the fingers (ulnar nerve), oppose the thumb and small finger (median nerve), and flex and extend the wrist (or the fingers, if in a cast) (radial nerve). •In the lower extremity, assess the patient's ability to perform dorsiflexion (peroneal nerve) and plantar flexion (tibial nerve). •Evaluate sensory function of the peroneal nerve by touching the web space between the great and second toes. •Stroke the plantar surface (sole) of the foot to assess sensory function of the tibial nerve. •Paresthesia (abnormal sensation [e.g., numbness, tingling]) and hypersensation/hyperesthesia may be reported by the patient. Partial or full loss of sensation (paresis/paralysis) may be a late sign of neurovascular damage. -Instruct patients to immediately report any changes in sensation or the ability to move the digits in the affected extremity.

intracranial pressure

-Understanding the dynamics associated with ICP is important in caring for patients with many different neurologic problems. -The skull is an enclosed space with three essential volume components: brain tissue, blood, and cerebrospinal fluid (CSF). -The intracellular and extracellular fluids of brain tissue make up approximately 78% of this volume. -Blood in the arterial, venous, and capillary network makes up 12% of the volume, and the remaining 10% is the volume of the CSF. -Intracranial pressure (ICP) is the hydrostatic force measured in the brain CSF compartment. -Under normal conditions in which intracranial volume remains relatively constant, the balance among the three components (brain tissue, blood, CSF) maintains the ICP. -Factors that influence ICP under normal circumstances are changes in (1) arterial pressure, (2) venous pressure, (3) intraabdominal and intrathoracic pressure (Valsalva), (4) posture, (5) temperature, and (6) blood gases, particularly CO2 levels. •The degree to which these factors increase or decrease the ICP depends on the brain's ability to adapt to changes. Regulation and Maintenance: -In applying the Monro-Kellie doctrine, the body can adapt to volume changes within the skull in three different ways to maintain a normal ICP. -First, compensatory mechanisms can include changes in the CSF volume. -The CSF volume can be changed by altering CSF absorption or production and by displacement of CSF into the spinal subarachnoid space. -Second, changes in intracranial blood volume can occur through the collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, and changes in venous outflow. -Third, tissue brain volume compensates through distention of the dura or compression of brain tissue. -Initially an increase in volume produces no increase in ICP as a result of these compensatory mechanisms. -However, the ability to compensate for changes in volume is limited. -As the volume increase continues, the ICP rises, and decompensation ultimately occurs, resulting in compression and ischemia. Increased ICP: -Increased ICP is a potentially life-threatening situation that results from an increase in any or all of the three components (brain tissue, blood, CSF) within the skull. -Elevated ICP is clinically significant because it diminishes CPP, increases risks of brain ischemia and infarction, and is associated with a poor prognosis. -Increased ICP can be caused by changes in any of the three components. -Common causes of increased ICP include a mass (e.g., hematoma, contusion, abscess, tumor) and cerebral edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation due to infection). -These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension, increase the formation and spread of cerebral edema Complications of Increased ICP: -Compression of the brainstem and cranial nerves may be fatal. -Herniation forces the cerebellum and brainstem downward through the foramen magnum. -If compression of the brainstem is unrelieved, respiratory arrest will occur due to compression of the respiratory control center in the medulla. -The major complications of uncontrolled increased ICP are inadequate cerebral perfusion and cerebral herniation. -To better understand cerebral herniation, two important structures in the brain must be described. -The falx cerebri is a thin wall of dura that folds down between the cortex, separating the two cerebral hemispheres. -The tentorium cerebelli is a rigid fold of dura that separates the cerebral hemispheres from the cerebellum. It is called the tentorium (meaning tent) because it forms a tentlike cover over the cerebellum. -Tentorial herniation (central herniation) occurs when a mass lesion in the cerebrum forces the brain to herniate downward through the opening created by the brainstem. -Uncal herniation occurs with lateral and downward herniation. -Cingulate herniation occurs with lateral displacement of brain tissue beneath the falx cerebri. Diagnostic Studies: -Diagnostic studies can be used to identify the cause of increased ICP. -Computed tomography (CT) and magnetic resonance imaging (MRI) are used to differentiate the many conditions that can cause increased ICP and to assess the effect of treatment. -Positron emission tomography (PET) is also used to diagnose the cause of increased ICP. -Additional tests include EEG, cerebral angiography, ICP measurement, brain tissue oxygenation measurement via the LICOX catheter, transcranial Doppler studies, and evoked potential studies. -In general, a lumbar puncture is not performed when a traumatic brain injury is suspected. The reason for this is that cerebral herniation could occur from the sudden release of the pressure in the skull from the area above the lumbar puncture. -In some institutions a hand-held near-infrared scanner (Infrascanner) is used to detect life-threatening intracranial bleeding. -The scanner directs a wavelength of light that can penetrate tissue and bone. -Blood from intracranial hematomas absorbs the light differently than other areas of the brain. Measurement of ICP: -ICP monitoring is used to guide clinical care when the patient is at risk for or has elevations in ICP. -It may be used in patients with a variety of neurologic insults, including hemorrhage, stroke, tumor, infection, or traumatic brain injury. -ICP should be monitored in patients admitted with a Glasgow Coma Scale (GCS) score of less than or equal to 8 and an abnormal CT scan or MRI (hematomas, contusion, edema). -These results indicate that the patient may have bleeding, contusion, edema, or other problems. -Need to be intubated if GCS is less than 8 -Patients with conditions known to elevate ICP usually undergo ICP monitoring in an ICU, except those with irreversible problems or advanced neurologic disease. -Multiple methods and devices are available to monitor ICP in various sites. Drug Therapy: -Mannitol (Osmitrol) (25%) is an osmotic diuretic given IV: •Mannitol acts to decrease the ICP in two ways: plasma expansion and osmotic effect. •An immediate plasma-expanding effect reduces the hematocrit and blood viscosity, thereby increasing CBF and cerebral oxygen delivery. •A vascular osmotic gradient is created by mannitol. Thus fluid moves from the tissues into the blood vessels. •Therefore the ICP is reduced by a decrease in the total brain fluid content. •Monitor fluid and electrolyte status when osmotic diuretics are used. -Hypertonic saline is another drug treatment used to manage increased ICP. •It produces massive movement of water out of edematous swollen brain cells and into blood vessels. •Hypertonic solution requires frequent monitoring of BP and serum sodium levels as intravascular fluid volume excess can occur. •Hypertonic saline has been shown to be just as effective as mannitol when treating increased ICP, and both are often used concurrently when caring for severely brain-injured patients. -Corticosteroids (e.g., dexamethasone [Decadron]) are used to treat vasogenic edema surrounding tumors and abscesses. •However, these drugs are not recommended for traumatic brain injury. •Corticosteroids stabilize the cell membrane and inhibit the synthesis of prostaglandins, thus preventing the formation of proinflammatory mediators. •Corticosteroids also improve neuronal function by improving CBF and restoring autoregulation. •Complications associated with the use of corticosteroids include hyperglycemia, increased incidence of infections, and gastrointestinal (GI) bleeding. •Regularly monitor fluid intake and sodium and glucose levels. •Perform blood glucose monitoring at least every 6 hours for any patient receiving corticosteroids until hyperglycemia is ruled out as a concern. •Patients receiving corticosteroids should concurrently be given antacids or histamine (H2)-receptor blockers (e.g., cimetidine [Tagamet], ranitidine [Zantac]) or proton pump inhibitors (e.g., omeprazole [Prilosec], pantoprazole [Protonix, Protonix IV]) to prevent GI ulcers and bleeding. -Metabolic demands such as fever (greater than 38°C), agitation/ shivering, pain, and seizures can also increase ICP. -The health care team should plan to reduce these metabolic demands in order to lower the ICP in the at-risk patient. -Monitor patients for seizure activity. -They may need to be placed on prophylactic antiseizure medication. •Emergent Seizure Activity: benzodiazepines (lorazepam) •Maintenance medications: phenytoin (Dilantin) -Fever should be well-controlled in order to maintain a temperature of 36° to 37°C by using antipyretics (e.g., acetaminophen), cool baths, cooling blankets, ice packs, or intravascular cooling devices as necessary without causing the patient to shiver or shake. -Shivering should be avoided as this increases the metabolic workload on the brain, and sedatives may be needed or a different type of cooling method selected. -Manage pain while being careful not to oversedate or medicate. -Finally, the patient should remain in a quiet and calm environment with minimal noise and interruptions. -Observe the patient for signs of agitation, irritation, or frustration. Also teach the caregiver and family about decreasing stimulation. -Coordinate with the interprofessional team to minimize procedures that may produce agitation. -Drug therapy for reducing cerebral metabolism may be an effective strategy to control ICP. Reducing the metabolic rate decreases the CBF and therefore the ICP. -High doses of barbiturates (e.g., pentobarbital [Nembutal], thiopental [Pentothal]) are used in patients with increased ICP refractory to other treatments. -Barbiturates decrease cerebral metabolism, causing a decrease in ICP as well as a reduction in cerebral edema and cerebral blood flow. -Not a good idea to give barbiturates Nursing Assessment: -Subjective data about the patient with increased ICP can be obtained from the patient, caregiver, or family who are familiar with the patient. -Describe the LOC by noting the specific behaviors observed. -Assess the LOC using the Glasgow Coma Scale. •The Glasgow Coma Scale (GCS) is a quick, practical, and standardized system for assessing the LOC. •The three areas assessed in the GCS are the patient's ability to (1) speak, (2) obey commands, and (3) open the eyes when a verbal or painful stimulus is applied. •Specific behaviors observed as responses to the testing stimulus are given a numeric value. •Your responsibility is to elicit the best response on each of the scales: the higher the scores, the higher the level of brain functioning. •The subscale scores are particularly important if a patient is untestable in one area. For example, severe periorbital edema may make eye opening impossible. •The total GCS score is the sum of the numeric values assigned to each of the three areas evaluated. •The highest GCS score is 15 for a fully alert person, and the lowest possible score is 3. •A GCS score of less than or equal to 8 is generally indicative of coma, and mechanical ventilation should be considered. •Plot the data on a graph, which can be used to determine whether the patient is stable, improving, or deteriorating. •The GCS offers several advantages in the assessment of the unconscious patient. •It allows different health care professionals to arrive at the same conclusion regarding the patient's status and can be used to discriminate between different or changing states. •Although the GCS is the gold standard assessment tool for LOC, other scales - such as the Full Outline of Unresponsiveness (FOUR) scale are also used in the clinical setting Clinical Manifestations: -Change in LOC: •Flattened affect (coma) •Change in vital signs -Cushing's triad (widened pulse pressure): •Hypertension, bradycardia, irregular respirations •Change in body temperature -Compression of Oculomotor Nerve/Cranial Nerves: •Unilateral pupil dilation •Sluggish or no response to light •Inability to move eye upward •Eyelid ptosis •Diplopia, blurred vision •EOM changes, pupillary reflex, corneal reflex -Motor Function: •Decrease in function •Hemiparesis/ hemiplegia •Decerebrate posturing (extensor) more serious change •Decorticate posturing (flexor) -Other Manifestations: •Headache, often continuous, worse in the morning •Vomiting not preceded by nausea •Projectile vomiting -As the ICP continues to rise, the patient manifests changes in motor ability. -A contralateral (opposite side of the mass lesion) hemiparesis or hemiplegia may develop, depending on the location of the source of the increased ICP. -If painful stimuli are used to elicit a motor response, the patient may localize to the stimuli or withdraw from it. -Noxious stimuli may also elicit decorticate (flexor) or decerebrate (extensor) posturing -Decorticate posture consists of internal rotation and adduction of the arms with flexion of the elbows, wrists, and fingers as a result of interruption of voluntary motor tracts in the cerebral cortex. Extension, internal rotation, and plantar flexion of the legs may also be seen. -A decerebrate posture may indicate more serious damage and results from disruption of motor fibers in the midbrain and brainstem. In this position, the arms are stiffly extended, adducted, and hyperpronated. There is also hyperextension of the legs with plantar flexion of the feet. Decerebrate is more serious and can lead to death -Know where seizure starts, how long it lasts, and if the client is post ictal -Major drug for a grand mal seizure is Ativan/ lorazepam Acute Care: -Maintain client airway -Elevate head of bed 30 degrees, suction only as needed, keep to a minimum -Minimize abdominal distention, NG tube for clients without facial or basal skull fractures (use OG instead) -Monitor ABG's, hypoxia: hypercapnia due to vasoactive action -Maintain ventilatory support -Opioids: fentanyl has less effect on brain perfusion/O2 -Propofol (Diprivan): short duration which allows more complete assessment -Dexmedetomidine(Precedex) -Neuromuscular blocking agents: paralyzers -Benzodiazepines: avoided most times. -Monitor IV fluids -Daily electrolytes (trend results) -Monitor for DI or SIADH (anything with brain trauma can cause these) -Monitor and minimize increases in ICP -Minimize valsalva, bearing down and arousing the client -Protection from self injury -Judicious use of restraints, sedatives -Seizure precautions -Maintain a quiet, non-stimulating environment -Psychological considerations -Maintain the patient with increased ICP in the head-up position. -The head should be maintained in a midline position, avoiding extreme neck flexion (neck flexion vasoconstricts). -This position can cause venous obstruction and contribute to elevated ICP. -Adjust the body position to decrease the ICP and to improve the CPP. -Elevation of the head of the bed promotes drainage from the head and decreases the vascular congestion that can produce cerebral edema. -However, raising the head of the bed above 30 degrees may decrease the CPP by lowering systemic BP. -Careful evaluation of the effects of elevation of the head of the bed on both the ICP and CPP is required. Position the bed so that it lowers the ICP while optimizing the CPP and other indices of cerebral oxygenation. -Take care to turn the patient with slow, gentle movements because rapid changes in position may increase the ICP. -Prevent discomfort in turning and positioning the patient because pain or agitation also increases pressure. -Increased intrathoracic pressure contributes to increased ICP by impeding the venous return. Thus coughing, straining, and the Valsalva maneuver should be avoided. -Avoid extreme hip flexion to decrease the risk of raising the intra-abdominal pressure, which increases ICP.

abdominal injury

Blunt Injuries: -Compression forces from seat belts, steering wheel can cause rupture of hollow organs and capsules of solid organs -Deceleration forces can tear organs from the peritoneum or blood vessels -Symptoms may be subtle Penetrating Injuries: -Stab wounds 3x more likely than gunshot wounds -Liver, bowel, and diaphragm most commonly injured Abdominal Compartment Syndrome: -Hypertension of the abdomen -Bleeding, fluid cause increased pressure which decreases perfusion to the organs -Leads to decreased CO, abdominal organ failure Concurrent Injuries: -Thoracic injuries -Rib fractures -Diaphragm injuries -Pelvic and lower extremity injuries Iceberg Effect: -Minimal external signs, symptoms, cues -Major internal organ damage and bleeding Symptoms: -VS changes indicating development of hypovolemic shock: •Hypotension, tachycardia, pale cool extremities, low urine output -Assess for: •Guarding, splinting •Hard, distended abdomen •Hypoactive or absent bowel sounds •Pain •Hematemesis •Hematuria •Bruits on auscultation: turbulent flow, damaged vessels Hepatic Injury: -5% of all admissions to ER -Graded by severity: 1-6, laceration to avulsion -Profuse bleeding -Right upper quadrant pain -Hypoactive or absent bowel sounds -Hypovolemic shock -May require surgical intervention Splenic Injury: -Most common from blunt trauma: 49% of all blunt injuries -Graded by severity: 1-5, laceration to shattered spleen -Signs of hypovolemic shock -Kehr's sign: pain in left shoulder -Rigidity and guarding -Bedrest if hemodynamically stable -May require surgical intervention Bowel Injuries: -Small bowel injury most common -Blunt and penetrating trauma -Shearing injury may cause avulsion of small bowel -Compression may cause rupture -Hypovolemic shock -Bleeding from rectum -Abdominal wall rigidity, guarding, pain Esophageal Injuries: -Rare -Associated with penetrating trauma -Neck, shoulder, chest, or abdominal pain -Subcutaneous air in neck -Frank blood from NG/Vomit Kidney Injuries: -Contusion from blunt trauma -10% of ER visit -Suspect renal injuries with posterior rib or lumbar vertebra fracture -Hematuria -Flank pain -Ecchymosis over site -Graded by severity Bladder and Urethral Injuries: -Blunt trauma Associated with pelvic fracture -Urethral injury more common in males -Suprapubic pain -Bleeding at the meatus -Urinary urgency -Abdominal rigidity, tenderness Nursing Assessment: -Cullen's Sign: •Bluish sign at umbilicus •Indicative of bleeding in the peritoneum -Grey Turner's Sign: bruising on the flanks indicating a retroperitoneal bleed (turns the corner and goes retroperitoneal) -Auscultation: bowel sounds in all 4 quadrants -Percussion: •Hyperresonance = Air •Dullness = Fluid -Palpation: •All 4 quadrants •Pelvis for instability •Anal sphincter for tone Diagnostic Procedures: -X-Rays -Labs: CBC, pregnancy, coags, UA, stool for blood -CT -FAST Exam: ultrasound that looks at 5 points in the peritoneal cavity, helps us see if there is free air or free fluid that should not be there -Angiography -Cystogram -Diagnostic peritoneal lavage for unstable clients: positive if return is colored, bloody Focused Assessment with Ultrasound/ Sonography for Trauma (FAST) Exam: -Used to diagnose free blood in the peritoneum after blunt trauma -Looks at 4 areas for free fluid: •Perihepatic •Perisplenic •Pelvis •Pericardium -94% effective -Test takes 4-5 minutes Nursing Interventions: -Emergency management -Maintain patent airway -2 large bore IVs -IVF or blood volume -Pain meds -Foley -NG -Cover open wounds -Antibiotics -Psychosocial support -Stabilize impaled objects -Surgical intervention -Monitor urinary output -Serial vital signs

fibromyalgia

Fibromyalgia: -Fibromyalgia is a chronic central pain syndrome marked by widespread, nonarticular musculoskeletal pain and fatigue with multiple tender points. -People with fibromyalgia may also experience nonrestorative sleep, morning stiffness, irritable bowel syndrome, and anxiety. -Commonly diagnosed -Major cause of disability -Affects 2% of the U.S. population -Fibromyalgia and systemic exertion intolerance disease (SEID) (formerly called chronic fatigue syndrome) share many common features -4-10 times more common in women -Disorder involving abnormal central processing nociceptive pain input -Abnormal sensory processing in CNS Clinical Manifestations and Complications: -The patient complains of a widespread burning pain that worsens and improves through the course of a day. -The patient often has trouble determining if pain occurs in the muscles, joints, or soft tissues. -Head or facial pain often results from stiff or painful neck and shoulder muscles. -The pain can accompany temporomandibular joint dysfunction, which affects an estimated one third of fibromyalgia patients. -Cognitive effects range from difficulty concentrating to memory lapses and a feeling of being overwhelmed when dealing with multiple tasks. -Many individuals report migraine headaches. -Physical examination typically reveals point tenderness at 11 or more of 18 identified sites. -Patients with fibromyalgia are sensitive to painful stimuli throughout the body and not just at the identified tender sites. -They may also experience pain in response to a stimulus that does not typically cause pain (allodynia). -In addition, point tenderness can vary from day to day. -Sometimes, the patient may respond to fewer than 11 tender points. -At other times, palpation of all sites may cause pain. -Depression and anxiety often occur and may require drug therapy. -Stiffness, nonrefreshing sleep, fatigue, and numbness or tingling in the hands or feet (paresthesia) often accompanies fibromyalgia. -Restless legs syndrome is also typical, with the patient describing an irresistible urge to move the legs when at rest or lying down. -Irritable bowel syndrome with manifestations of constipation and/or diarrhea, abdominal pain, and bloating is common. -Patients may also experience difficulty swallowing, perhaps because of problems in esophageal smooth muscle function. -Increased frequency of urination and urinary urgency, in the absence of a bladder infection, are typical complaints. -Women with fibromyalgia may experience more difficult menstruation with a worsening of disease symptoms during this time. Diagnostic Studies: -A definitive diagnosis of fibromyalgia is often difficult to establish. -Lack of knowledge about the disease and its manifestations among HCPs may also cause delays in diagnosis and treatment. -Laboratory results in most cases serve to rule out other suspected disorders. -Occasionally a low ANA titer is seen, but it is not considered diagnostic. -Muscle biopsy may reveal a nonspecific moth-eaten appearance or fiber atrophy. -Fibromyalgia if two criteria are met: •Pain is experienced in 11 of 18 tender points on palpation •History of widespread pain is noted for at least 3 months -Fatigue, cognitive symptoms, somatic symptoms help establish diagnosis -Subsequent classification by ACR -Nontender point diagnostic criteria: •Symptom severity scale •Widespread pain index Interprofessional Care: -Symptomatic treatment -Requires high level of patient motivation -Patient teaching -Rest can help the pain, aching, and tenderness -Drug therapy for chronic widespread pain: Pregabalin (Lyrica), gabapentin (Neurontin), Duloxetine (Cymbalta), Milnacipin (Savella) -Low-dose tricyclic antidepressants (TCAs), SSRIs, or benzodiazepines -Muscle relaxants -Nonopioid analgesics -Zolpidem (Ambien), skeptical about giving it to an older patient Nursing Management: -Patients with fibromyalgia may consider limiting their consumption of sugar, caffeine, and alcohol because these substances may be muscle irritants. -Vitamin and mineral supplements may be appropriate to combat stress, correct deficiencies, and support the immune system. -However, unproven miracle diets or supplements should be carefully investigated by the patient and discussed with the HCP before using them. -The patient should understand that some foods and supplements may cause serious or even dangerous side effects when mixed with certain drugs. -Pain and the related symptoms of fibromyalgia can cause significant stress. -Patients with fibromyalgia may not cope well with stress. -Effective relaxation strategies include biofeedback, imagery, meditation, and cognitive behavioral therapy. -Patients need to receive initial training for these interventions, but they can then continue to practice in their own homes. -Psychologic counseling (individual or group) and a support group may also be beneficial for the patient with fibromyalgia.

bug injuries

-Fleas, black widow, ticks, fire ants -Animals, spiders, snakes, and insects cause injury and even death by biting or stinging. -Morbidity is a result of either direct tissue damage or lethal toxins. -Direct tissue damage is a product of animal size, characteristics of the animal's teeth, and strength of the jaw. -Tissue is lacerated, crushed, or chewed, while teeth, fangs, stingers, spines, or tentacles release toxins that have local or systemic effects. -Death associated with animal bites is due to blood loss, allergic reactions, or lethal toxins. -Little kids can go into anaphylactic shock from red ant bites -The Hymenoptera family includes bees, yellow jackets, hornets, wasps, and fire ants. -Stings can cause mild discomfort or life-threatening anaphylaxis. -Venom may be cytotoxic, hemolytic, allergenic, or vasoactive -Ticks live throughout the United States, but are most common in the northwestern, Rocky Mountain, and northeastern regions. -Conditions associated with tick bites include Lyme disease, Rocky Mountain spotted fever, and tick paralysis. -The infected tick or the release of neurotoxin causes the disease. -Ticks release neurotoxic venom as long as the tick head attaches to the body. -Therefore safe removal of the tick is essential for effective treatment. -Use forceps or tweezers to grasp the tick close to the point of attachment and pull upward in a steady motion. -After you remove the tick, clean the skin with soap and water. -Do not use a hot match, petroleum jelly, nail polish, or other products to remove the tick, since these measures may cause a tick to salivate, thus increasing the risk for infection. -Lyme disease is the most common tick-borne disease in the United States. -Symptoms appear within days of a bite from the Ixodid (hard) tick that has been attached for at least 48 hours -The first stage of this disease begins with flu-like symptoms (e.g., headache, stiff neck, fatigue). -Some patients may develop a characteristic bull's eye rash (i.e., a circular area of redness 5 cm or more in diameter). -The rash, if it develops, will disappear even if the patient is not treated. -Rocky Mountain spotted fever is caused by Rickettsia rickettsii, a bacterium that is spread to humans by the Ixodid tick. -It has an incubation period of 2 to 14 days. -A pink, macular rash appears on the palms, wrists, soles, feet, and ankles within 10 days of exposure. -Other symptoms include fever, chills, malaise, myalgias, and headache. -Diagnosis is often difficult in the early stages, and without treatment the disease can be fatal. -Antibiotic therapy with doxycycline is the treatment of choice. Hymenoptera Stings: -Bees, yellow jackets, hornets, wasps, and fire ants -Mild discomfort or life-threatening anaphylaxis-number of stings worsens -Venom may be cytotoxic, hemolytic, allergenic, or vasoactive Tick Bites: -Lyme disease-48 hour attachment, flu-like, bullseye rash-long term immune systemic response causes chronic illness -Rocky Mountain spotted fever (2-14 days): pink macular rash: palms, wrists, feet, can be fatal -Safe removal: tweezers at the head/stinger area -Doxycycline treatment of choice -Make sure to get the head of the tick out

focal injury

-Focal injury can be minor to severe and can be localized to an area of injury. -Focal injury consists of lacerations, contusions, hematomas, and cranial nerve injuries. Lacerations: -Lacerations involve actual tearing of the brain tissue and often occur in association with depressed and open fractures and penetrating injuries. -Tissue damage is severe, and surgical repair of the laceration is impossible due to the nature of brain tissue. -Medical management consists of antibiotics until meningitis is ruled out, and preventing secondary injury related to increased ICP. -If bleeding is deep into the brain tissue, focal and generalized signs develop. -Intracerebral hemorrhage is generally associated with cerebral laceration. -This hemorrhage manifests as a space-occupying lesion accompanied by unconsciousness, hemiplegia on the contralateral side, and a dilated pupil on the ipsilateral side. As the hematoma expands, signs of increased ICP become more severe. -Subarachnoid hemorrhage and intraventricular hemorrhage can also occur secondary to head trauma. Contusion: -A contusion is the bruising of the brain tissue within a focal area. -It is usually associated with a closed head injury. -A contusion may contain areas of hemorrhage, infarction, necrosis, and edema, and frequently occurs at a fracture site. -Contusions may continue to bleed or rebleed and appear to "blossom" on subsequent CT scans of the brain. Bleeding worsens the neurologic outcome. -Neurologic assessment may demonstrate focal as well as generalized manifestation, depending on the size and location of the contusion. -Seizures can occur as a result of a brain contusion, particularly when the injury involves the frontal or temporal lobes. -Anticoagulant use and coagulopathy are associated with increased hemorrhage, more severe head injury, and an increased mortality rate. -This is especially important when considering older individuals who are taking anticoagulants. -If they fall, their contusion is likely to be more severe due to the use of anticoagulants. -Risk for falls should be assessed in all patients taking anticoagulants. -With contusion, the phenomenon of coup-contrecoup injury is often noted and can range from minor to severe. -Damage from coup-contrecoup injury occurs when the brain moves inside the skull due to high-energy or high-impact injury mechanisms. -Contusions or lacerations occur both at the site of the direct impact of the brain on the skull (coup) and at a secondary area of damage on the opposite side away from injury (contrecoup), leading to multiple contused areas. -Contrecoup injuries tend to be more severe, and overall patient prognosis depends on the amount of bleeding around the contusion site. -Monitor for seizures -Potential for increased hemorrhage if on anticoagulants Epidural Hematoma: -An epidural hematoma results from bleeding between the dura and inner surface of the skull. -An epidural hematoma is a neurologic emergency and is usually associated with a linear fracture crossing a major artery in the dura, causing a tear. -It can have a venous or an arterial origin. -Venous epidural hematomas are associated with a tear of the dural venous sinus and develop slowly. -With arterial hematomas, the middle meningeal artery lying under the temporal bone is often torn. -Hemorrhage occurs into the epidural space, which lies between the dura and the inner surface of the skull. -Because this is an arterial hemorrhage, the hematoma develops rapidly. -Classic signs of an epidural hematoma typically include an initial period of unconsciousness at the scene, with a brief lucid interval followed by a decrease in LOC. -Other manifestations may be a headache, nausea and vomiting, or focal findings. -Rapid surgical intervention to evacuate the hematoma and prevent cerebral herniation, along with medical management for increasing ICP, can dramatically improve outcomes. Subdural Hematoma: -A subdural hematoma occurs from bleeding between the dura mater and arachnoid layer of the meninges. -It can be acute, subacute, or chronic -A subdural hematoma usually results from injury to the brain tissue and its blood vessels. -The veins that drain from the surface of the brain into the sagittal sinus are the source of most subdural hematomas. -Because a subdural hematoma is usually venous in origin, the hematoma may be slower to develop. -However, a subdural hematoma may be caused by an arterial hemorrhage, in which case it develops more rapidly. Subdural hematomas may be acute, subacute, or chronic. Acute Subdural Hematoma: -An acute subdural hematoma manifests within 24 to 48 hours of the injury. -The signs and symptoms are similar to those associated with brain tissue compression in increased ICP and include decreasing LOC and headache. -The size of the hematoma determines the patient's clinical presentation, as well as prognosis. -The patient's appearance may range from drowsy and confused to unconscious. -The ipsilateral pupil dilates and becomes fixed if ICP is significantly elevated. -Blunt force injuries that produce acute subdural hematomas also may cause significant underlying brain injury, resulting in cerebral edema. -The resulting increase in ICP from the cerebral edema can cause increased morbidity and mortality risk despite surgical intervention to evacuate the hematoma. Subacute Subdural Hematoma: -A subacute subdural hematoma usually occurs within 2 to 14 days of the injury. -After the initial bleeding, a subdural hematoma may appear to enlarge over time, as the breakdown products of the blood draw fluid into the subdural space. Chronic Subdural Hematoma: -A chronic subdural hematoma develops over weeks or months after a seemingly minor head injury. -Chronic subdural hematomas are more common in older adults due to a potentially larger subdural space as a result of brain atrophy. -With atrophy, the brain remains attached to the supportive structures, but tension is increased, and it is subject to tearing. -The larger size of the subdural space also accounts for the presenting complaint to be focal symptoms (specific to a certain area of the brain), rather than the signs of increased ICP. -Chronic alcoholics are also prone to cerebral atrophy and subsequent development of subdural hematoma due to an increased incidence of falls. -Delay in diagnosis of a subdural hematoma in the older adult can be attributed to symptoms that mimic other health problems in persons of this age group, such as somnolence, confusion, lethargy, and memory loss. -The manifestations of a subdural hematoma are often misinterpreted as vascular disease (stroke, transient ischemic attack [TIA]) and dementia. Intracerebral Hematoma: -Intracerebral hematoma occurs from bleeding within the brain tissue and occurs in approximately 16% of head injuries. -It usually occurs within the frontal and temporal lobes, possibly from the rupture of intracerebral vessels at the time of injury. -The size and location of the hematoma is a key determinant of the patient's outcome.

muscular dystrophy (MD)

-Group of genetic diseases -Progressive symmetric wasting of skeletal muscles with no evident neurological involvement -Differ in types, onset, progression and genetic link Diagnostics: -Creatine kinase -EMG testing -Muscle fiber biopsy: fat and connective tissue deposits and dystrophin -ECG: cardiomyopathy; dysrhythmias (most frequent cause of death) -Progressive weakness and deformity -Ambulatory devices, braces, PT, activity -Heart failure -Respiratory failure: ventilator-CPAP dependent with tracheostomy -Supportive treatment: steroids delay progression for up to 2 years

encephalitis

-Acute inflammation of the brain -Can be fatal 1400 deaths annually -Usually viral -Transmitted by mosquitoes: •West Nile, measles, chicken pox, mumps, HSV or CMV in immunocompromised Nonspecific symptom onset: -Fever, HA, N/V -Altered LOC: mild or coma -Many variation of neuro symptoms: •Hemiparesis, seizures, nerve palsies, tremors •Memory, personality, amnesia, dysphagia -CT, MRI -Test for viral antigens -Patient care: •Antiviral medications: acyclovir for HSV •Antiseizure medications -Prevention: •Mosquito control •Early treatment with antivirals and supportive care

blunt chest trauma injury

Pulmonary Contusion: -Erythema/ Ecchymosis -Dyspnea -Chest wall pain -Crepitus -Hypoventilation -Decreased breath sounds Cardiac Contusion: -Bruise to the heart tissue -MVC, falls, sports injuries -CPR -EKG abnormalities -Chest pain -Chest wall bruising -Irregular heart beat -Hypotension Rib and Sternal Fractures: -Pain -Dyspnea -Chest wall bruising -Crepitus or bony deformity -Patient splints the chest for comfort Flail Chest: -Two or more broken ribs adjacent to one another -Segment moves independently during respiration -Dyspnea -Chest wall pain -Paradoxical chest movement

hypothermia

-Core temperature less than 95 degrees Fahrenheit (35 degrees Celsius) -Core temperatures less than 89.6 degrees Fahrenheit (32 degrees Celsius) are potentially life threatening -Occurs when heat produced by the body cannot compensate for heat lost to the environment. -Most body heat is lost as radiant energy, with the greatest loss from the head, thorax, and lungs (with each breath). -Wet clothing increases evaporative heat loss 5 times greater than normal; immersion in cold water (e.g., drowning) increases evaporative heat loss 25 times greater than normal. -Environmental exposure to freezing temperatures, cold winds, and wet terrain plus physical exhaustion, inadequate clothing, and inexperience predisposes individuals to hypothermia. -Older adults are more prone to hypothermia because of decreased body fat, diminished energy reserves, decreased basal metabolic rate, decreased shivering response, decreased sensory perception, chronic medical conditions, and drugs that alter body defenses. -Hypothermia mimics cerebral or metabolic disturbances, causing ataxia, confusion, and withdrawal, so the patient may be misdiagnosed. -Peripheral vasoconstriction is the body's first attempt to conserve heat. -As cold temperatures persist, shivering and movement are the body's only mechanisms for producing heat. -Patients with mild hypothermia (93.2° to 96.8° F [34° to 36° C]) have shivering, lethargy, confusion, rational to irrational behavior, and minor heart rate changes. -Moderate hypothermia (89.6° to 93.2° F [32° to 34° C]) causes rigidity, bradycardia, slowed respiratory rate, BP obtainable only by Doppler, metabolic and respiratory acidosis, and hypovolemia. -Shivering diminishes or disappears at core temperatures of 89.6° F (32° C). -As core temperature drops, metabolic rate decreases two or three times. -The cold myocardium is extremely irritable, making it vulnerable to dysrhythmias (e.g., atrial and ventricular fibrillation). -Decreased renal blood flow decreases glomerular filtration rate, which impairs water reabsorption and leads to dehydration. -The hematocrit increases as intravascular volume decreases. -Cold blood becomes thick and acts as a thrombus, placing the patient at risk for stroke, myocardial infarction, pulmonary emboli, and renal failure. -Decreased blood flow leads to hypoxia, anaerobic metabolism, lactic acid accumulation, and metabolic acidosis. -Severe hypothermia (below 89.6° F [32° C]) makes the person appear dead and is a potentially life-threatening situation. -Metabolic rate, heart rate, and respirations are so slow that they may be difficult to detect. -Reflexes are absent, and the pupils fixed and dilated. -Profound bradycardia, ventricular fibrillation, or asystole may be present. -Every effort is made to warm the patient to at least 86° F (30° C) before the person is pronounced dead. -The cause of death is usually refractory ventricular fibrillation. -The patient is not truly dead until they are warm; so keep trying to bring them back while they are still cold even if they look dead -Hypothermia protocol: can preserve organ function Treatment of hypothermia: -Manage and maintain ABCs -Rewarm patient -Correct dehydration and acidosis -Treat cardiac dysrhythmias Mild hypothermia treatment: -Passive external (spontaneous) rewarming: •Move patient to warm, dry place; remove damp clothing; use radiant lights; place warm blankets on patient -Active external (surface) rewarming: •Fluid- or air-filled warming blankets, warm water immersion Moderate to severe hypothermia treatment: -Active internal or core rewarming: •Refers to application of heat directly to the core •Heated, humidified oxygen (up to 111.2ºF [44ºC]) •Warmed IV fluids (up to 98.6ºF [37ºC]) •Peritoneal lavage with warmed fluids (up to 113ºF[45ºC]) •Extracorporeal circulation with cardiopulmonary bypass, rapid fluid infuser, and hemodialysis -Rewarm core before extremities -Risks of rewarming: •Afterdrop •Hypotension •Dysrhythmias -Discontinue rewarming once core temperature reaches 89.6º to 93.2º F (32º to 34º C)

spinal cord injury (SCI)

-Spinal cord injury (SCI) is caused by trauma or damage to the spinal cord. -It can result in either a temporary or permanent alteration in the function of the spinal cord. -About 12,500 Americans experience SCIs each year. -The number of persons living with SCI in the United States is about 276,000 persons. -Young adult men between ages 16 and 30 years have the greatest risk for SCI. -There has also been an increase in the number of older adults with SCIs. -This increase is related to people with SCI living longer and older age at the time of injury. -With improved treatment strategies, even the very young patient with an SCI can anticipate a long life. -The potential for disruption of individual growth and development, altered family dynamics, economic loss in terms of employment issues, and the high cost of rehabilitation and long-term health care make spinal cord injury a major problem. -Although many people with SCIs can care for themselves independently, those with the highest level of injury may require round-the-clock care at home or in a long-term care facility. -Spinal cord injuries are usually from trauma. -The most common causes are motor vehicle collisions (38%), falls (30%), violence (14%), sports injuries (9%), and other miscellaneous causes (9%). -The spinal cord is wrapped in tough layers of dura and is rarely torn or transected by direct trauma. -Spinal cord injury can result from cord compression by bone displacement, interruption of blood supply to the cord, or traction resulting from pulling on the cord. -Penetrating trauma, such as gunshot and stab wounds, can cause tearing and transection. -The initial mechanical disruption of axons as a result of stretch or laceration is referred to as the primary injury -Hanging is an example of traction from pulling on the cord -Secondary injury: ongoing, progressive damage that occurs after initial injury; several theories exist on what causes ongoing damage -The resulting hypoxia reduces the oxygen levels below the metabolic needs of the spinal cord. -Lactate metabolites and an increase in vasoactive substances, including norepinephrine, serotonin, and dopamine, occur. -High levels of these vasoactive substances cause vasospasms and hypoxia with subsequent necrosis. -Unfortunately, the spinal cord has minimal ability to adapt to vasospasm. -Spinal shock may occur following acute SCI and is characterized by decreased reflexes, loss of sensation, absent thermoregulation, and flaccid paralysis below the level of the injury. -This syndrome lasts days to weeks and may mask post-injury neurogenic shock -SCI is classified by: •Mechanism of injury •Level of injury •Degree of injury -Major mechanisms of injury are: •Flexion: ruptures the posterior ligaments •Hyperextension: ruptures the anterior ligaments •Flexion-rotation: often results in tearing of ligamentous structures that normally stabilize the spine •Extension-rotation •Compression: crush the vertebrae and force bony fragments into the spinal canal Level of Injury: -Skeletal level of injury is the vertebral level with the most damage to vertebral bones and ligaments. -Neurologic level is the lowest segment of the spinal cord with normal sensory and motor function on both sides of the body. -The level of injury may be cervical, thoracic, lumbar, or sacral. -Cervical and lumbar injuries are most common because these levels are associated with the greatest flexibility and movement. -If the cervical cord is involved, paralysis of all four extremities occurs, resulting in tetraplegia (formerly quadriplegia). -The degree of impairment in the arms following cervical injury depends on the level of injury. -The lower the level, the more function is retained in the arms. -If the thoracic, lumbar, or sacral spinal cord is damaged, the result is paraplegia (paralysis and loss of sensation in the legs). -C4 injury: tetraplegia, results in complete paralysis below the neck -C6 injury: results in partial paralysis of hands and arms as well as lower body -T6 injury: paraplegia, results in paralysis below the chest -L1 injury: paraplegia, results in paralysis below the waist Degree of Injury: -The degree of spinal cord involvement may be either complete or incomplete (partial). -Complete cord involvement results in total loss of sensory and motor function below the level of the injury. -Incomplete cord involvement results in a mixed loss of voluntary motor activity and sensation and leaves some tracts intact. -The degree of sensory and motor loss depends on the level of the injury and the specific damaged nerve tracts. -Five major syndromes are associated with incomplete injuries: •Central cord syndrome •Anterior cord syndrome •Brown-Séquard syndrome •Cauda equina syndrome •Conus medullaris syndrome -Incomplete SCI: anterior cord syndrome -Incomplete SCI: Brown-Séquard Syndrome Incomplete SCI Central Cord Syndrome: -Caused from damage to the central spinal cord. -Occurs most commonly in the cervical cord region. -More common in older adults. -Motor weakness and sensory loss are present in upper extremities. -Lower extremities not usually affected -Dysesthetic burning pain is felt in upper extremities. Clinical Manifestations: -The manifestations of SCI are generally related to the direct result of trauma that causes cord compression, ischemia, edema, and possible cord transection. -Manifestations of SCI are related to the level and degree of injury. -The patient with an incomplete injury may demonstrate a mixture of manifestations. -Sequelae are more serious with higher energy Respiratory System: -Respiratory complications closely correspond to the level of the injury. -Cervical injuries above the level of C4 present special problems because of the total loss of respiratory muscle function. -Injury or fracture below the level of C4 results in diaphragmatic breathing if the phrenic nerve is functioning. -Even if the injury is below C4, spinal cord edema and hemorrhage can affect the function of the phrenic nerve and cause respiratory insufficiency. -Hypoventilation and impairment of the intercostal muscles leads to a decrease in vital capacity and tidal volume. -Cervical and thoracic injuries cause paralysis of abdominal muscles and often the intercostal muscles. -Thus the patient cannot cough effectively enough to remove secretions, increasing the risk for aspiration, atelectasis and pneumonia. -Neurogenic pulmonary edema may occur secondary to a dramatic increase in sympathetic nervous system activity at the time of injury, which shunts blood to the lungs. -In addition, pulmonary edema may occur in response to fluid overload. -To improve respiratory function for patients with spinal cord injury, resistive inspiratory muscle training may be effective. Cardiovascular System: -Any cord injury above T6 leads to dysfunction of the sympathetic nervous system. -This leads to neurogenic shock -The result is bradycardia, peripheral vasodilation, and hypotension. -Peripheral vasodilation causes a relative hypovolemia because of the increase in the capacity of the dilated veins. -It also reduces venous return of blood to the heart. -Cardiac output then decreases, leading to hypotension. -Other injuries can also cause hemorrhagic shock and further reduce BP. -It is important to identify all causes of hypotension in the person with SCI. Urinary System: -Urinary dysfunction occurs in the majority of patients following SCI. -Neurogenic bladder describes any type of bladder dysfunction related to abnormal or absent bladder innervation. -After spinal cord shock resolves, depending on the completeness of the SCI, patients usually have some degree of neurogenic bladder. -Normal voiding requires nervous system coordination of urethral and pelvic floor relaxation, with simultaneous contraction of the detrusor muscle. -Depending on the injury, a neurogenic bladder may (1) have no reflex detrusor contractions (flaccid, hypotonic), (2) have hyperactive reflex detrusor contractions (spastic), or (3) lack coordination between detrusor contraction and urethral relaxation (dyssynergia). -Common problems with a neurogenic bladder include urgency, frequency, incontinence, inability to void, and high bladder pressures resulting in reflux of urine into the kidneys. -Patients with neurogenic bladder usually get a suprapubic catheter -Acute phase: •Urinary retention •Bladder atonic, overdistended, fails to empty •Indwelling catheter -Postacute phase: •Bladder may become hyperirritable •Loss of inhibition from brain •Reflex emptying and failure to store urine Gastrointestinal System: -Decreased GI motor activity contributes to gastric distention and development of paralytic ileus. -Gastric emptying may be delayed, especially in patients with higher level SCI. -Excessive release of HCl acid in the stomach may cause stress ulcers. -Dysphagia may also be present in patients who require mechanical ventilation, tracheostomy, and anterior spine surgery. -Intra-abdominal bleeding may be difficult to diagnose because the person with SCI may not experience pain or tenderness. -Continued hypotension and decreased hemoglobin and hematocrit may indicate bleeding. -Expanding girth of the abdomen may also be noted. -FAST exam: abdominal ultrasound Integumentary System: -The risk for skin breakdown over bony prominences in areas of decreased or absent sensation is a major consequence of immobility related to SCI. -Pressure ulcers can occur quickly and can lead to major infection and sepsis. -Poikilothermism is the adjustment of the body temperature to the room temperature. -It occurs in SCI because interruption of the sympathetic nervous system prevents peripheral temperature sensations from reaching the hypothalamus. -Spinal cord disruption is also marked by decreased ability to sweat or shiver below the level of the injury, which also affects the ability to regulate body temperature. -The degree of poikilothermism depends on the level of injury. -High cervical injuries are associated with a greater loss of the ability to regulate temperature than are thoracic or lumbar injuries. -People assume the temperature of where they are Peripheral Vascular Problems: -Venous thromboembolism (VTE) is a common problem accompanying SCI during the first 3 months. -Detecting a DVT may be difficult in a person with an SCI because the usual signs and symptoms, such as pain and tenderness, will not be present. -Pulmonary embolism is one of the leading causes of death in patients with SCI. -Nociceptive Pain: •Musculoskeletal pain is dull or aching, worsens with movement •Visceral pain in thorax, abdomen, pelvis: dull, tender, or cramping -Neuropathic Pain: •Located at or below level of injury •Hot, burning, tingling, pins and needles, cold, shooting •May be extremely sensitive to stimuli Diagnostic Studies: -CT scan is the preferred imaging study to diagnose the location and degree of injury as well as degree of spinal canal compromise. -Cervical x-rays are obtained when CT scan is not readily available. -However, visualizing C7 and T1 on a cervical x-ray is often difficult, and the ability to fully evaluate cervical spine injury is compromised. -MRI is used to assess for soft tissue injury, neurologic changes, unexplained neurologic deficits, or worsening of neurologic condition. -Perform a comprehensive neurologic examination with assessment of the head, chest, and abdomen for additional injuries or trauma. -Patients with cervical injuries who demonstrate altered mental status may also need a CT angiogram to rule out vertebral artery damage. -Duplex Doppler ultrasound, impedance plethysmography, venous occlusion plethysmography, venography, and clinical examination are used to diagnose DVT. Interprofessional Care: -Immediate goals •Patent airway •Adequate ventilation/breathing •Adequate circulating blood volume (ABCs) •Prevent extension of spinal cord damage (secondary injury) -Immobilization: •Rigid cervical collar •Backboard with straps •Spinal immobilization with penetrating trauma not recommended -Maintain systolic BP >90mm Hg Acute Care: -Compared to cervical injury, patients with SCI of the thoracic and lumbar vertebrae require less intense support. -At this level of injury, respiratory compromise is not as severe and bradycardia is usually not a problem. -Other problems are treated symptomatically. -Obtain a history, with emphasis on how the incident occurred. -Assess the extent of injury perceived by the patient or by the emergency response system (ERS) personnel immediately after the event. -Initial assessment (which usually occurs in the emergency department) includes managing the person's ABCs and vital signs to ensure the airway is secure, oxygenation saturation (SaO2) is greater than 90%, and SBP is greater than 90 mm Hg. -Appropriate medical interventions and diagnostics are implemented to ensure the patient is hemodynamically stable. -A complete neurologic assessment is completed using the ASIA tool -Brain injury and/or vertebral artery injury: •History of unconsciousness •Signs of concussion •Increased intracranial pressure -Musculoskeletal injuries -Trauma to internal organs -Move the patient in alignment as a unit (logroll) during transfers and when repositioning to prevent further injury. -Monitor respiratory, cardiac, urinary, and GI functions. -The patient may go directly to surgery after initial immobilization or to the intensive care unit (ICU) for monitoring and management. -Stabilization of injured spinal segment: •Eliminates damaging motion •Prevent secondary damage -Decompression: traction or realignment -Early realignment: •Closed reduction •Craniocervical traction Surgical Therapy: -Surgical treatment is used following acute SCI to fix the instability and decompress the spinal cord. -The type of surgery depends on the severity and level of the injury, mechanism of injury, and location and degree of compression. -Early spinal cord decompression may reduce secondary injury and thus improve the patient's outcome. -Surgery within the first 24 hours after SCI is safe and associated with improved neurologic outcome. -Surgery to stabilize the spine can be performed from the back of the spine (posterior approach) or from the front of the spine (anterior approach). In some cases, both approaches may be needed. -Fusion involves attaching metal screws, plates, or other devices to the bones of the spine to help keep them aligned. -This procedure is usually done when two or more vertebrae have been injured. -Small pieces of bone may also be attached to the injured bones to help them fuse into one solid piece. -The bone used for this procedure can be obtained from the patient's spinal bone harvested during surgery, from another bone in the patient's body (autologous), or from donor bone (allograft). Drug Therapy: -Low-molecular-weight heparin (e.g., enoxaparin [Lovenox]) is used to prevent VTE unless contraindicated. -Contraindications include internal bleeding, abnormal kidney function, and recent surgery. -Vasopressor agents, such as phenylephrine (Neo-Synephrine) or norepinephrine (Levophed), are used in the acute phase as adjuvants to treatment. -These agents are used to maintain the mean arterial pressure (MAP) at a level greater than 85-90 mm Hg to improve perfusion to the spinal cord. -Use of vasopressors has significant risk of complications, including ventricular tachycardia, troponin elevation, metabolic acidosis, and atrial fibrillation. -Because drug metabolism is altered in patients with an SCI, drug interactions may occur. -Differences in drug metabolism correlate with level and completeness of injury, with greater change apparent following cervical cord injury than injury at lower spinal levels. Fluid and Nutritional Maintenance: -During the first 48 to 72 hours after the injury, the GI tract may stop functioning (paralytic ileus). -A nasogastric tube must be inserted if ileus occurs. -Because the patient cannot have oral intake, carefully monitor fluid and electrolyte status. -Nutrition should be started within the first 72 hours following injury. -Specific solutions and additives are ordered based on individual requirements. -Due to severe catabolism, a high-protein, high-calorie diet is needed for energy and tissue repair. -If the patient cannot be fed through the GI system, either orally or through a feeding tube placed into the duodenum, parenteral nutrition should be initiated to reduce nitrogen losses that occur during the hypermetabolic state. Bladder Management: -Immediately after the injury, urine is retained because of the loss of autonomic and reflex control of the bladder and sphincter (neurogenic bladder). -Because there is no sensation of fullness, overdistention of the bladder can result in reflux into the kidney and cause renal failure. -Bladder overdistention may even result in rupture of the bladder. -Thus, an indwelling catheter may be inserted as soon as possible after injury. -Ensure the patency of the catheter by frequent inspection and irrigation if necessary. -In some institutions a physician's order is required for this procedure. -Strict aseptic technique for catheter care is essential to prevent infection. -During the period of indwelling catheterization, encourage a large fluid intake. -Check the catheter to prevent kinking and ensure free flow of urine. -Catheter-acquired urinary tract infection (CAUTI) is a common problem. -The best method for preventing UTIs is regular and complete bladder drainage. -After the patient is stabilized, assess the best means of managing long-term urinary function. Usually the patient is started on an intermittent catheterization program. -Intermittent catheterization should be done 4-6 times daily to prevent bacterial overgrowth resulting from urinary stasis. -Keep urine residuals under 500 mL to prevent bladder distention. -If the urine is cloudy or has a strong odor or if the patient develops symptoms of a UTI (e.g., chills, fever, malaise), send a specimen for culture. Temperature: -Because the patient has no vasoconstriction, piloerection (erection of body hair), or heat loss through perspiration below the level of injury, temperature control is largely external to the patient. -Temperature control is external -Monitor the environment closely to maintain an appropriate temperature. -Also regularly monitor the patient's body temperature. -Do not use excessive covers or unduly expose the patient (such as during bathing). -If an infection with high fever develops, more extensive methods for temperature control may be needed (e.g., a cooling blanket). Stress Ulcers: -Stress ulcers can occur in the patient with an SCI because of the physiologic response to severe trauma and psychologic stress. -Peak incidence of stress ulcers is 6 to 14 days after injury. -Test stool and gastric contents daily for blood and monitor the hematocrit for a slow drop. -Histamine (H2)-receptor blockers (e.g., ranitidine [Zantac], famotidine [Pepcid]) or proton pump inhibitors (e.g., pantoprazole [Protonix], omeprazole [Prilosec]) may be given prophylactically to decrease the secretion of HCl acid and prevent the occurrence of ulcers during the initial phase. Effect on Person and Family: -Depression after SCI is common and disabling. -Patients with SCIs may feel an overwhelming sense of loss. -They may temporarily lose control over everyday life activities as they depend on others for ADLs and for life-sustaining measures. -Patients may believe that they are useless and burdens to their families. -At a life stage when independence is often of great importance, they may be totally dependent on others. -With recent advances in rehabilitation, the patient is often independent physically and discharged from the rehabilitation center before completing the grief process. -The goal of recovery is related more to adjustment than to acceptance. -Adjustment implies the ability to go on with living with certain limitations. -Although the patient who is cooperative and accepting is easier to treat, expect a wide fluctuation of emotions from a patient with SCI. -Your role in grief work is to allow mourning as part of the rehabilitation process. -Maintaining hope is important during the grieving process and should not be interpreted as denial. -Sympathy not helpful -Encourage patient participation -Consistency of care -Psychiatric consult if needed -Caregiver and family counseling -Support group Gerontologic Considerations: -Because of our aging population and increased work and recreational activities among older adults, more of them are experiencing SCI. -Falls are the leading cause of SCI for people age 65 and older. -Older adults with traumatic injuries experience more complications than younger patients, are hospitalized longer, and have higher mortality rates. -Health promotion and screening are important for the older patient with an SCI. -Daily skin inspections and UTI prevention measures are critical. -Monthly breast examinations for women and regular prostate cancer screening for men are recommended. -Cardiovascular disease is the most common cause of morbidity and mortality among older adults with SCI. -The lack of sensation, including chest pain, in persons with high-level injuries may mask acute myocardial ischemia. -Altered autonomic nervous system function and decreases in physical activity can place patients at risk for cardiovascular problems, including hypertension. -To decrease the risk of injuries, instruct patients and caregivers on fall prevention strategies (e.g., using a stepstool or a long-handled reacher to access high shelves, install handrails on stairs). -Rehabilitation for the older person with SCI may take longer because of preexisting conditions and poorer health status at the time of initial injury. -An interprofessional team approach to rehabilitation is essential in preventing secondary complications associated with SCI, especially in older adults.

systemic lupus erythematosus

-Systemic lupus erythematosus (SLE) is a multisystem inflammatory autoimmune disease -It is a complex disorder of multifactorial origin resulting from interactions among genetic, hormonal, environmental, and immunologic factors. Affects: -Skin -Joints -Serous membranes: pleura, pericardium -Renal system -Hematologic system -Neurologic system -Marked by an unpredictable course with alternating periods of remission and worsening disease -Most cases in women of childbearing years -More common in African Americans, Asian Americans, Hispanics, and Native Americans than in Caucasians -Overaggressive autoimmune reactions directed against constituents of: cell nucleus, single- and double-stranded DNA, activation of B and T cells -Etiology is unknown Probable Causes: -Genetic influence -Hormones -Environmental factors -Certain medications: •At least 40 medications currently in use may trigger SLE, such as procainamide (Pronestyl), hydralazine (Apresoline), and quinidine (Quiniglut). Clinical Manifestations: -Severity of SLE is extremely variable -Ranges from a relatively mild disorder to rapidly progressive disease affecting many body systems -Most commonly affects skin, muscles, lining of lungs, heart, nervous tissue, and kidneys -The specific manifestations of SLE depend on which cell types or organs are involved. -No characteristic pattern occurs in the progressive involvement of SLE. -Any organ can be affected by an accumulation of circulating immune complexes. -Generalized complaints such as fever, weight loss, arthralgia, and excessive fatigue may precede an exacerbation of disease activity. -Other signs of SLE include anemia, mild leukopenia, and thrombocytopenia Dermatologic Problems: -Vascular skin lesions can appear anywhere but are most likely to develop on sun-exposed areas. -Severe skin reactions can occur in people who are sensitive to sunlight (photosensitivity). -The classic butterfly rash over the cheeks and bridge of the nose occurs in 55% to 85% of patients at some time during the disease. -About 20% of patients have discoid (round coin-shaped) lesions. -A small number of patients have persistent lesions, photosensitivity, and mild systemic disease in a syndrome known as subacute cutaneous lupus. -Oral or nasopharyngeal ulcers occur in up to one third of patients with SLE. -Alopecia is also common, with or without related scalp lesions. The hair may grow back during remission, but hair loss may be permanent over lesions. The scalp becomes dry, scaly, and atrophied. Musculoskeletal Problems: -Arthritis occurs in about 95% of patients with SLE. -Pain in multiple joints (polyarthralgia) with morning stiffness is often the patient's first complaint. It may precede the onset of multisystem disease by many years. -Diffuse swelling occurs with joint and muscle pain, and some stiffness. -Lupus-related arthritis is generally nonerosive, but it may cause deformities (e.g., swan neck deformity of the fingers, ulnar deviation, subluxation with joint hyperlaxity). -Increased risk of bone loss and fracture Cardiopulmonary Problems: -Tachypnea and cough in patients with SLE suggest presence of lung disease. -Pleurisy is also possible. -Cardiac involvement may include dysrhythmias due to fibrosis of the sinoatrial and atrioventricular nodes. -This indicates advanced disease, contributing greatly to the morbidity and mortality of SLE. -Pericarditis can also occur. -Clinical factors such as hypertension and hypercholesterolemia require aggressive treatment and careful monitoring. -People with SLE are at risk for secondary antiphospholipid syndrome. -This is a disorder of coagulation that leads to clots in the arteries and veins with related risk of stroke, gangrene, and heart attack due to emboli. Renal Problems: -About 75% of persons with SLE experience kidney damage (lupus nephropathy). -Renal involvement is usually evident within the first 2 years after diagnosis. -Mild proteinuria to rapidly progressive glomerulonephritis -Scarring and permanent damage can lead to end-stage kidney disease (leading cause of death). -The importance of obtaining a renal biopsy is controversial, but findings can help guide treatment. -Although renal failure is the leading cause of death for patients with SLE, effective treatments are available. -These typically include corticosteroids (prednisone, methylprednisolone), cytotoxic agents (cyclophosphamide [Cytoxan]), and immunosuppressive agents (azathioprine [Imuran], cyclosporine, and mycophenolate mofetil [CellCept]). -Rituximab (Rituxan) and eculizumab (Soliris) are being studied as possible treatments. -Oral prednisone or pulsed IV methylprednisolone may also be used as an intervention for LN, especially in the initial treatment period when cytotoxic agents have not yet taken effect. Nervous System Problems: -Generalized or focal seizures of the CNS occur in as many as 15% of patients with SLE by the time of diagnosis. -Seizures are generally controlled by corticosteroids or antiseizure drugs. -Peripheral neuropathy can lead to sensory and motor deficits. -Cognitive dysfunction may result from the deposit of immune complexes within the brain. -It is marked by disordered thinking, disorientation, and memory deficits. -Various psychiatric disorders are reported in SLE, including depression, mood disorders, anxiety, and psychosis. However, they may also be related to the stress of having a major illness or to associated drug therapies. -Occasionally SLE may cause a stroke or aseptic meningitis. -Headaches are also common and can become severe during a disease flare. Hematologic Problems: -Abnormal blood conditions are common in SLE due to formation of antibodies against blood cells. -Anemia, leukopenia, thrombocytopenia, and coagulation disorders (excessive bleeding or clotting) are often present. -Many patients with SLE benefit from high-intensity treatment with warfarin. Infection: -Patients with SLE appear to have increased susceptibility to infections. -Risk may be due to: •Impaired ability to phagocytize invading bacteria •Deficient production of antibodies •Immunosuppressive effects of many antiinflammatory drugs. -Infection is a major cause of death, with pneumonia is the most common infection. -Fever may indicate an underlying infection rather than lupus activity alone. -Vaccinations are generally safe for patients with SLE. -However, patients being treated with corticosteroids or cytotoxic drugs must avoid live virus vaccines. Diagnostic Studies: -No specific test is diagnostic for SLE, but a variety of abnormalities may be present in the blood. -SLE is primarily diagnosed on criteria: history, physical examination, and laboratory findings -Anti-nucleic antibody (ANA): •SLE is marked by the presence of ANA in 97% of persons with the disease. •Anti-DNA antibodies are found in half the persons with SLE, but lupus can still be present if these antibodies are not identified. •The anti-Smith (Sm) antibodies are found in 30% to 40% of persons with lupus and are almost always considered diagnostic. -Nearly 30% of people with lupus will have antiphospholipid antibodies. -Antibodies to histone are most often seen in people with drug-induced SLE. -Elevated ESR and CRP are not diagnostic of SLE, but may be used to monitor disease activity and effectiveness of therapy. Interprofessional Care: -A major challenge in the treatment of SLE is managing the active disease while preventing complications of treatments that cause tissue damage. -Survival is influenced by several factors, including age, race, sex, socioeconomic status, co-morbid conditions, and disease severity. -Prognosis can be improved with early diagnosis, ongoing assessment, and prompt recognition of serious organ involvement, and effective therapeutic regimens. Drug Therapy: -NSAIDs continue to be an important intervention, especially for patients with mild arthralgia or arthritis. -Careful patient monitoring during long-term NSAID use must include potential for GI and renal effects. -Antimalarial agents such as hydroxychloroquine (Plaquenil) and chloroquine (Aralen) are often used to treat fatigue and moderate skin and joint problems. •They modulate the immune system, but do not cause immunosuppression. •These drugs may also reduce occurrence of flares. -Use of corticosteroids should be limited. However, tapering doses of IV methylprednisolone may manage severe flares of polyarthritis. -Steroid-sparing immunosuppressants such as methotrexate can serve as an alternative treatment. -High doses of corticosteroids may be especially appropriate for the patient with severe cutaneous SLE. •Immunosuppressive drugs such as azathioprine and cyclophosphamide may be used to reduce the need for long-term corticosteroid therapy. -Clinical trials are currently investigating the effect of various medications on SLE management. •These include agents that interfere with the immune response such as abatacept, and hormones (prasterone [Prestara]) to combat corticosteroid-induced osteoporosis. •Lenalidomide, a chemical derivative of thalidomide, can improve cutaneous lupus without adverse neurologic effects. Nursing Diagnoses: -Assess patient's physical, psychologic, and sociocultural problems with long-term management of SLE -Evaluate effect of pain and fatigue on ability to perform ADLs -Fatigue related to chronic inflammation and altered immunity -Impaired skin integrity related to photosensitivity, skin rash, and alopecia -Impaired comfort related to symptoms of illness, treatment side effects, and potential variable and unpredictable disease progression Overall Goals: -Have satisfactory pain management -Adhere to therapeutic regimen to achieve maximum symptom management -Demonstrate awareness of and avoid activities that worsen the disease -Maintain optimal role function and positive self-image Acute Care: -Unpredictable nature of SLE presents many challenges for the patient and caregiver -Physical, psychologic, and sociocultural problems linked to long-term management -During a disease flare, patient may quickly become very ill -Record severity of symptoms and response to therapy -Observe for: •Fever pattern •Joint inflammation •Limitation of motion •Location and degree of discomfort •Fatigue Psychosocial Issues: -Supportive therapies to help patient cope with the disease -Inform patient and caregiver that SLE has good prognosis for most people -Stress importance of planning recreational and occupational activities -The young adult may find sun restrictions and physical limitations difficult to follow. -Help the patient develop and accomplish reasonable goals for improving or maintaining mobility, energy, and self-esteem. -Families worry about hereditary aspects and want to know if their children will also have SLE. -Many couples require pregnancy and sexual counseling. -Individuals making decisions about marriage and careers worry about how SLE will interfere with their plans. Lupus and Pregnancy: -Infertility can result: renal involvement, high-dose corticosteroids, immunosuppressive drugs -Women with serious SLE should be counseled against pregnancy -The patient should understand that spontaneous abortion, stillbirth, and intrauterine growth retardation are common problems with pregnancy. -They occur because immune complexes are deposited in the placenta and inflammation occurs in placental blood vessels. -For the best outcome, pregnancy should be planned at a point when the disease activity is minimal. -Flares are common during the postpartum period. -Therapeutic abortion offers the same risk of postdelivery exacerbation as carrying the fetus to term Health Promotion: -Prevention of SLE is not currently possible -Education of health professionals and the community to create a clear understanding of the disease and need for early diagnosis and treatment Ambulatory Care: -Emphasize importance of patient involvement for successful home management -Help patient understand that strong adherence to treatment is no guarantee against flares -Reduce exposure to precipitating factors: fatigue, sun exposure, emotional stress, infection, drugs, and surgery -Expected Outcomes: -Use energy conservation techniques -Adapt lifestyle to current energy -Maintain skin integrity with the use of topical treatments -Prevent disease flare with the use of sunscreens and limited sun exposure

brain tumors

Benign Brain Tumors: -Benign brain tumors do not contain cancer cells: usually, benign tumors can be removed, and they seldom grow back. -The border or edge of a benign brain tumor can be clearly seen. -Cells from benign tumors do not invade tissues around them or spread to other parts of the body. -However, benign tumors can press on sensitive areas of the brain and cause serious health problems. -Unlike benign tumors in most other parts of the body, benign brain tumors are sometimes life threatening. -Very rarely, a benign brain tumor may become malignant. Malignant Brain Tumors: -Malignant brain tumors are generally more serious and often are life threatening. -They may be primary (the tumor originates from the brain tissue) or secondary (metastasis from other tumors elsewhere in the body). -They are likely to grow rapidly and invade the surrounding healthy brain tissue. Risk Factors: -Being male -Race -Age -Family history -Being exposed to radiation or certain chemicals at work Signs and Symptoms: -Symptoms related to increased intracranial pressure such as: •Decrease in level of consciousness such as confusion and lethargy. •Headache most common in the early morning and made worse by coughing or straining •Vomiting •Papilledema (edema of optic nerve) and visual disturbance •Alteration in mental status -Localized Symptoms Such As: •Aphasia •Personality changes as in case of frontal lobe tumor •Sensory defects (smell, hearing) •Seizures •Motor abnormalities Diagnosis of Brain Tumor: -Physical exam -Neurological examination -Brain CT scan -MRI on brain -Angiogram -Spinal tap -Biopsy -Won't do lumbar puncture for ICP, but will do spinal tap for brain tumor Treatment of Brain Tumor: -A variety of medical treatment modalities, including chemotherapy and radiotherapy, are used alone or in combination with surgical resection. -Supportive care includes: •Steroids •Anticonvulsant drugs

thoracic injury

Mechanisms of Injury: -Acceleration and deceleration forces: tearing of aorta and vessels as body stops, organs do not •"Coup-contracoup" -First and second rib fractures can severely injure the pulmonary and cardiac tissues underneath -Falls -Crush Injuries -Violence -Motor Vehicle Crashes -Be concerned about pneumothorax and hemothorax as well -Ineffective ventilation due to disruption in the anatomical structures in the thoracic cavity -Tears in the bronchial tree -Rib/sternal fractures -Pain -Lung contusion -Impaled object in the chest Ineffective Circulation: -Internal or external hemorrhage due to injury to the great vessels -Blunt trauma can lead to decrease myocardial contractility and cardiac output -Pericardial tamponade -Air in thoracic cavity can cause venous congestion Diagnostic Procedures: -Chest X-Ray -CT -Bronchoscopy -EKG -Cardiac enzymes, CBC -Central venous pressure Management of Care: -Airway -Respiratory effort: rate, depth -Symmetrical chest wall movement -Jugular vein distension -Look for chest wall injuries, bruising -Percuss for dullness: hemothorax -Palpate: •Chest wall, clavicles, and neck for crepitus, edema, and pain •Central and peripheral pulses •Assess for tracheal deviation •Blood pressures in upper and lower extremities for aortic injuries

drowning

Submersion: -Submersion injury results when a person becomes hypoxic as the result of submersion in a liquid, usually water. -More than 50,000 submersion events and approximately 4,000 deaths from drowning occur each year in the United States. -Most of the victims are children younger than 5 years of age or boys and men between ages 15 and 25. -The primary risk factors for submersion injury include inability to swim, use of alcohol or drugs, trauma, seizures, hypothermia, stroke, and child neglect. Drowning: -Drowning is the process of experiencing respiratory impairment after submersion in water or other fluid. -Submersion in cold water (below 32° F [0° C]) may slow the progression of hypoxic brain injury. -Most drowning victims do not aspirate any liquid due to laryngospasm. -If liquid is aspirated, it is in small amounts (e.g., 4 mL/kg). -Drowning victims who do aspirate water develop pulmonary edema. -Regardless of what type of fluid is aspirated, the end result can be acute respiratory distress syndrome. -Lack of oxygen causes drowning deaths, not water in the lungs -No one is declared dead until they are warmed up Pathophysiology of Submersion Injury: -The osmotic gradient caused by aspirated fluid leads to fluid imbalances in the body. -Hypotonic freshwater is rapidly absorbed into the circulatory system through the alveoli. -Freshwater is often contaminated with chlorine, mud, or algae. -This causes the breakdown of lung surfactant, fluid seepage, and pulmonary edema. -Hypertonic saltwater draws fluid from the vascular space into the alveoli, impairing alveolar ventilation and resulting in hypoxia. -The body attempts to compensate for hypoxia by shunting blood to the lungs. -This results in increased pulmonary pressures and deteriorating respiratory status. -More and more blood is shunted through the alveoli. -However, the blood is not adequately oxygenated, and hypoxemia worsens. -This can result in cerebral injury, edema, and brain death. -Aggressive resuscitation efforts (e.g., airway and ventilation management), especially in the prehospital phase, improve survival of drowning victims. Assessment: -Pulmonary: •Ineffective breathing •Dyspnea •Respiratory distress •Respiratory arrest •Crackles, rhonchi •Cough with pink-frothy sputum •Cyanosis -Cardiac: •Tachycardia •Bradycardia •Dysrhythmia •Hypotension •Cardiac arrest -Other: •Panic •Exhaustion •Coma •Coexisting illness (e.g., MI) or injury (e.g., cervical spine injury) •Core temperature slightly elevated or below normal depending on water temperature and length of submersion Interprofessional Care: -Treatment of submersion injuries: •Correct hypoxia •Correct acid-base and fluid imbalances •Support basic physiologic functions •Rewarm if hypothermia present -Initially evaluate: •Airway, cervical spine, breathing, circulation, (ABCs) -Mechanical ventilation with PEEP or CPAP: •Improves gas exchange in presence of pulmonary edema •Ventilation and oxygenation are primary techniques for treating respiratory failure -Deterioration in neurologic status: •Cerebral edema, worsening hypoxia, profound acidosis -Complications can develop even when patients are initially symptom free -Minimum of 23 hours of hospital observation

bacterial meningitis

-Acute inflammation of meningeal tissue surrounding brain and spinal cord -Usually occurs in fall, winter, or early spring -Often secondary to viral respiratory disease -Older adults and persons who are debilitated are more often affected than is the general population. -College students living in dormitories and individuals living in institutions (e.g., prisoners) have a high risk for contracting meningitis. -Untreated bacterial meningitis has a mortality rate near 100%, and must be reported to the Centers for Disease Control (CDC). -Anyone admitted to the hospital with a diagnosis of meningitis will be put in isolation (because it can be bacterial or viral) Etiology and Pathophysiology: -Streptococcus pneumoniae -Neisseria meningitides has at least 13 different subtypes (serogroups) with five of them (A, B, C, Y, W) causing most cases. -Haemophilus influenzae was once the most common cause. -However, the use of H. influenzae vaccine has resulted in a significant decrease in meningitis related to this organism. -A basilar skull fracture can lead to bacterial meningitis -The inflammatory response to the infection tends to increase CSF production with a moderate increase in ICP. -In bacterial meningitis the purulent secretions produced quickly spread to other areas of the brain through the CSF and cover the cranial nerves and other intracranial structures. -All patients with meningitis must be observed closely for manifestations of increased ICP, which is thought to be a result of swelling around the dura and increased CSF volume. -Cerebral edema and increased ICP become problematic -If process extends into parenchyma If concurrent encephalitis is present Clinical Manifestations: -Fever -Severe headache -Nausea, vomiting -Nuchal rigidity -Coma associated with poor prognosis: •Occurs in 5% to 10% of cases -Photophobia -↓ LOC -Signs of ↑ ICP: •Seizures occur in 1/3 of all cases •Headache worsens •Vomiting and irritability may occur -If the infecting organism is a meningococcus, a skin rash is common, and petechiae may be seen on the trunk, lower extremities, and mucous membranes. -A Tumbler test can be done by pressing the base of a drinking glass against the rash. -The rash does not blanch or fade under pressure. Complications: -Hemiparesis, dysphasia, and hemianopsia may also occur. -These signs usually resolve over time. -If they do not, a cerebral abscess, subdural empyema, subdural effusion, or persistent meningitis is suspected. -Hemianopsia: blindness in one eye; if you're helping a patient ambulate, walk with them on their blind side -Headaches may occur for months after the diagnosis of meningitis until the irritation and inflammation have completely resolved. -It is important to implement pain management for chronic headaches. -A noncommunicating hydrocephalus may occur if the exudate causes adhesions that prevent the normal flow of CSF from the ventricles. -CSF reabsorption by the arachnoid villi may also be obstructed by the exudate. In this situation, surgical implantation of a shunt is the only treatment. -Waterhouse-Friderichsen syndrome is a complication of meningococcal meningitis. -The syndrome is manifested by petechiae, disseminated intravascular coagulation (DIC), adrenal hemorrhage, and circulatory collapse. -DIC and shock, which are some of the most serious complications of meningitis, are associated with meningococcemia -Acute cerebral edema may cause seizures, CN III palsy, bradycardia, hypertensive coma, and death Nursing Assessment: -Initial assessment should include: •Vital signs •Neurologic assessment •Fluid intake and output •Evaluation of lungs and skin Nursing Diagnosis: -Decreased intracranial adaptive capacity related to decreased cerebral perfusion or increased ICP -Risk for ineffective cerebral tissue perfusion related to reduction of blood flow and cerebral edema -Hyperthermia related to infection -Acute pain related to headache and muscle aches Diagnostic Studies: -When a patient has manifestations suggestive of bacterial meningitis, a blood culture and CT scan should be done. -Diagnosis is usually verified by doing a lumbar puncture with analysis of the CSF. -A lumbar puncture should be completed only after the CT scan has ruled out an obstruction in the foramen magnum in order to prevent a fluid shift resulting in herniation. -Specimens of the CSF, sputum, and nasopharyngeal secretions are taken for culture before the start of antibiotic therapy to identify the causative organism. -A Gram stain is done to detect bacteria. -After a lumbar puncture, they should lay flat for 4-6 hours; we take out 3-4L of CSF so encourage fluids that are vasoconstrictors (coffee, tea, Coke products) -The predominant white blood cell type in the CSF during bacterial meningitis is neutrophils. -X-rays of the skull may demonstrate infected sinuses. CT scans and MRI may be normal in uncomplicated meningitis. -In other cases, CT scans may reveal evidence of increased ICP or hydrocephalus. Interprofessional Care: -Bacterial meningitis is a medical emergency. -Rapid diagnosis based on history and physical examination is crucial because the patient is usually in a critical state when health care is sought. -When meningitis is suspected, antibiotic therapy is begun after the collection of specimens for cultures, even before the diagnosis is confirmed -Ampicillin, penicillin, vancomycin, cefuroxime (Ceftin), cefotaxime (Claforan), ceftriaxone (Rocephin), ceftizoxime (Cefizox), and ceftazidime (Ceptaz) are some commonly prescribed drugs for treating bacterial meningitis. -Dexamethasone (a corticosteroid) may also be prescribed before or with the first dose of antibiotics. -Collaborate with the HCP to manage the headache, fever, and nuchal rigidity often associated with meningitis. Acute Care: -Revolve around the nursing diagnoses of: •↓ Intracranial adaptive capacity •Risk for ineffective cerebral perfusion •↑ Fever •Acute pain -The patient with bacterial meningitis is usually acutely ill. -The fever is high, and head pain is severe. -Irritation of the cerebral cortex may result in seizures. -The changes in mental status and LOC depend on the degree of increased ICP. -Assess and record vital signs, neurologic status, fluid intake and output, skin, and lung fields at regular intervals based on the patient's condition. -Assist the patient to a position of comfort, often curled up with the head slightly extended. The head of the bed should be slightly elevated, when permitted after lumbar puncture. -The presence of a familiar person at the bedside may have a calming effect. -Get the head of the bed up at least 30 degrees to help decrease ICP, also give oxygen because it vasodilates -Mannitol is an osmotic diuretic that helps reduce swelling -Be careful with intake and output: increased fluid, increased ICP -No hip flexion: don't put pressure on aorta and on vena cava -Have patient eat 6 small meals as opposed to 3 big ones to prevent the stomach from putting pressure on the vena cava -Close observation and assessment -Provide relief for head and neck pain -Position for comfort -Darkened room and cool cloth over eyes for photophobia -Minimize environmental stimuli: •Mental distortion and hypersensitivity are typical •Caring and unhurried, gentle, efficient care -Provide safety -The patient with bacterial meningitis is usually acutely ill. -The fever is high, and head pain is severe. -Irritation of the cerebral cortex may result in seizures. -The changes in mental status and LOC depend on the degree of increased ICP. -Assess and record vital signs, neurologic status, fluid intake and output, skin, and lung fields at regular intervals based on the patient's condition. -Assist the patient to a position of comfort, often curled up with the head slightly extended. The head of the bed should be slightly elevated, when permitted after lumbar puncture. -The presence of a familiar person at the bedside may have a calming effect. Nursing Implementation: -Observe and record seizures: •Prevent injury •Administer antiseizure medications -Vigorously manage fever: •Fever increases cerebral edema and the frequency of seizures •Neurologic damage may result from high, prolonged fever -If the fever is resistant to aspirin or acetaminophen, more vigorous means are necessary, such as a cooling blanket. -Care should be taken not to reduce the temperature too rapidly because shivering may result, causing a rebound effect and increasing the temperature. -Wrap the extremities in soft towels or a blanket covered with a sheet to reduce the occurrence of shivering, which can raise ICP. -If a cooling blanket is not available or desirable, tepid sponge baths with water may be effective in lowering the temperature. -Protect the skin from excessive drying and injury and prevent breaks in the skin. -Assess for dehydration: •Evaluate fluid intake and output •Compensate for diaphoresis in replacement fluids -Maintain therapeutic blood levels of antibiotics -Respiratory isolation until cultures are negative -Calculate replacement fluids as 800 mL/day for respiratory losses and 100 mL for each degree of temperature above 100.4°F (38°C). -Supplemental feeding (e.g., enteral nutrition) to maintain adequate nutritional intake may be necessary. -Meningococcal meningitis is highly contagious, whereas other causes of meningitis may pose minimal to no infection risk with patient contact. -However, standard precautions are essential to protect the patient and the nurse. Ambulatory Care: -Progressive ROM exercises and warm baths for muscle rigidity -Ongoing assessment for recovery of vision, hearing, cognitive skills, motor, and sensory abilities -Tend to signs of anxiety and stress of family and caregivers -Provide for several weeks of convalescence -Increase activity as tolerated -Stress adequate nutrition: high-protein, high-calorie diet small, frequent feedings. -Encourage adequate rest and sleep -Residual effects can result in sequelae such as dementia, seizures, deafness, hemiplegia, and hydrocephalus. -Appropriate referrals as indicated Health Promotion: -Prevention of respiratory tract infections through vaccination programs for pneumococcal pneumonia and influenza is important. -Meningococcal vaccines are available that protect against all serogroups of meningococcal disease that are most commonly seen in the United States, but they will not prevent all cases. -Three kinds of meningococcal vaccines available in the United States include: •Meningococcal conjugate vaccines (MCV4) (Menactra, MenHibrix, Menveo) •Meningococcal polysaccharide vaccine (MPSV4) (Menomune) •Serogroup B meningococcal vaccines (Bexsero and Trumenba) -Early, vigorous treatment of respiratory tract and ear infections -Prophylactic antibiotics for anyone exposed to bacterial meningitis

fat embolism

-Fat embolism syndrome (FES) is characterized by systemic fat globules from fractures that are distributed into tissues, lungs, and other organs after a traumatic skeletal injury. -FES is a contributory factor in mortality associated with fractures. -The fractures that most often are associated with FES include those of the long bones, ribs, tibia, and pelvis. -FES can also occur after total joint replacement, spinal fusion, liposuction, crush injuries, and bone marrow transplantation. Two theories about fat embolism exist: -According to the mechanical theory, fat emboli may originate from the fat that is released from the marrow of injured bone. •The fat then enters the systemic circulation where it embolizes to other organs such as the brain, where it can obstruct. •As fat droplets lodge in small blood vessels, local ischemia and inflammation occur. -The biochemical theory suggests hormonal changes caused by trauma or sepsis stimulate the systemic release of free fatty acids (e.g., chylomicrons) that form the fat emboli. -Early recognition of FES is crucial to prevent a potentially lethal course. -Most patients manifest symptoms within 24 to 48 hours after the injury. -Severe forms have occurred within hours of injury. -Fat emboli in the lungs cause a hemorrhagic interstitial pneumonitis with signs and symptoms of acute respiratory distress syndrome (ARDS), such as chest pain, tachypnea, cyanosis, dyspnea, apprehension, tachycardia, and decreased partial pressure of arterial O2 (PaO2). -These symptoms are caused by poor oxygen exchange. -Changes in mental status (a result of hypoxemia) are also part of the classic triad of signs and symptoms. -Investigate memory loss, restlessness, confusion, elevated temperature, and headache so central nervous system involvement is not mistaken for alcohol withdrawal or acute head injury. -Petechiae located on the neck, anterior chest wall, axilla, buccal membrane, and conjunctiva of the eye may help distinguish fat emboli from other problems. They may appear due to intravascular thromboses caused by decreased oxygenation. However, petechiae are only seen in 25% to 50% of cases of FES. -The clinical course of a fat embolus may be rapid and acute. -Frequently the patient expresses a feeling of impending disaster. -In a short time, skin color changes from pallor to cyanosis, and the patient may become comatose. -No specific laboratory examinations are available to aid in the diagnosis. -However, certain diagnostic abnormalities may be present. -These include fat cells in the blood, urine, or sputum; a decrease of PaO2 to less than 60 mm Hg; ST segment and T-wave changes on ECG; a decrease in the platelet count and hematocrit levels; and an elevated erythrocyte sedimentation rate (ESR). -A chest x-ray may show bilateral pulmonary infiltrates. Treatment: -Treatment for fat embolism is directed at prevention. -Careful immobilization and handling of a long bone fracture is probably the most important factor in the prevention of fat embolism. -Reposition the patient as little as possible before fracture immobilization or stabilization because of the danger of dislodging fat droplets into the general circulation. -Management of FES is mostly supportive and related to management of symptoms. -Treatment includes fluid resuscitation to prevent hypovolemic shock, correction of acidosis, and replacement of blood loss. -Encourage coughing and deep breathing. -Administer O2 to treat hypoxia. -Intubation or intermittent positive pressure ventilation may be considered if a satisfactory PaO2 cannot be obtained with supplemental oxygen alone. -Some patients may develop pulmonary edema, ARDS, or both, leading to increased mortality rate. -Most persons survive FES with few sequelae.

compartment syndrome

-Compartment syndrome is a condition in which swelling causes increased pressure within a limited space (muscle compartment). -Because the fascia surrounding the muscle has limited ability to stretch, continued swelling can cause pressure that compromises the function of blood vessels, nerves, and/or tendons in the compartment. -Capillary perfusion is reduced below a level needed for tissue viability. -Compartment syndromes usually involve the leg but can also occur in any muscle group (e.g., arm, shoulder, buttock, abdomen). -Two basic causes of compartment syndrome are •(1) Decreased compartment size resulting from restrictive dressings, splints, casts, excessive traction, or premature closure of fascia and •(2) Increased compartment contents related to bleeding, inflammation, edema, or IV infiltration. -Edema can create sufficient pressure to obstruct circulation and cause venous occlusion, which further increases edema. -Arterial flow is eventually compromised, causing ischemia in the extremity. -As ischemia continues, muscle and nerve cells are destroyed. -Fibrotic tissue eventually replaces healthy tissue. -Contracture, disability, and loss of function can occur. -Delays in diagnosis and treatment result in irreversible muscle and nerve ischemia. -The extremity may become functionally useless or severely impaired extremity. -Compartment syndrome is usually associated with trauma, fractures (especially of long bones), extensive soft tissue damage, and crush injury. -Fractures of the distal humerus and proximal tibia are the most common fractures associated with compartment syndrome. -Early recognition and treatment is essential -Compartment syndrome may occur initially from the physiologic response of the body to the injury, or it may be delayed for several days after the original insult or injury. -Ischemia can occur within 4 to 8 hours after the onset of compartment syndrome. One or more of the following six Ps are characteristic of compartment syndrome: 1)Pain out of proportion to the injury and that is not managed by opioid analgesics, and pain on passive stretch of muscle traveling through the compartment 2)Increasing pressure in the compartment 3)Paresthesia (numbness and tingling) 4)Pallor, coolness, and loss of normal color of the extremity 5)Paralysis or loss of function 6)Pulselessness (diminished or absent peripheral pulses) Interprofessional Care: -Prompt, accurate diagnosis of compartment syndrome is critical. -Perform and document regular neurovascular assessments on all patients with fractures, especially those with injury of the extremities or soft tissue injuries in these areas. -Early recognition and effective treatment of compartment syndrome are essential to avoid permanent damage to muscles and nerves. -Carefully assess the location, quality, and intensity of the pain. Evaluate the patient's level of pain on a scale of 0 to 10. -Pain unrelieved by drugs and out of proportion to the level of injury is one of the first indications of impending compartment syndrome. -Paresthesia is also an early sign. -Notify the HCP immediately of these changes in the patient's condition. -If the source of pressure is relieved (e.g., cast is cut [bivalve] or dressing loosened by order of the HCP), pain and paresthesia typically decrease and compartment syndrome is avoided. -Pulselessness and paralysis are later signs. -Because of the possibility of muscle damage, assess urine output. -Myoglobin released from damaged muscle cells precipitates and causes obstruction in renal tubules. -This condition results in acute tubular necrosis and acute kidney injury. Common signs are dark reddish brown urine and clinical manifestations associated with acute kidney injury. -Elevation of the extremity may lower venous pressure and slow arterial perfusion. -With suspected compartment syndrome, the extremity should not be elevated above the heart level. -Similarly, the application of cold compresses may cause vasoconstriction and exacerbate compartment syndrome (NO ice) -Surgical decompression (e.g., fasciotomy) of the involved compartment may be necessary. The fasciotomy site is left open for several days to ensure adequate soft tissue decompression. -Infection resulting from delayed wound closure is a potential problem after fasciotomy. -In severe cases of compartment syndrome, an amputation may be required.

Guillain-Barre Syndrome

-Guillain-Barré syndrome (GBS), once thought to be a single entity characterized by inflammatory peripheral neuropathy, is a combination of clinical features with various forms of presentation and multiple pathologic processes. -Most cases of GBS do not require admission to the critical care unit. -However, the prototype of GBS, known as acute inflammatory demyelinating polyradiculoneuropathy (AIDP), involves a rapidly progressive, ascending peripheral nerve dysfunction, which leads to paralysis that may produce respiratory failure. -Because of the need for ventilatory support, AIDP is one of the few peripheral neurologic diseases that necessitates care in a critical care environment. -In this discussion, all references to GBS pertain to the AIDP prototype. -The annual incidence of GBS is 1.8 cases per 100,000 persons. -It occurs more often in men and is the most commonly acquired demyelinating neuropathy. -The cause of GBS remains unknown, but the syndrome involves an immune-mediated response involving cell-mediated immunity and development of immunoglobulin G (IgG) antibodies. -Most patients report a viral infection 1 to 3 weeks before onset, usually involving the upper respiratory tract. -Most patients report a viral infection 1 to 3 weeks before onset, usually involving the upper respiratory tract -More often in men and is the most commonly acquired demyelinating neuropathy -ICU management needed with acute ascending case: "Toes to Nose" with respiratory paralysis -With no curative treatment available, the medical management of GBS is limited. -The disease must run its course, which is characterized by ascending paralysis that advances over 1 to 3 weeks and then remains at a plateau (peak) for 2 to 4 weeks. -The plateau stage is followed by descending paralysis and return to normal or near-normal function. -The main focus of medical management is the support of bodily functions and the prevention of complications. -Plasmapheresis and intravenous immune globulin (IVIG) are used to treat GBS. IVIG has emerged as the preferred therapy because of convenience and availability. -Mechanical ventilation prevents complications -The nursing management of the patient with GBS incorporates a variety of nursing diagnoses and interventions. -The goal of nursing management is to support all normal body functions until the patient can do so on his or her own. -Although the condition is reversible, the patient with GBS requires extensive long-term care, because recovery can be a long process. -Nursing interventions focus on maintaining surveillance for complications, initiating rehabilitation, facilitating nutritional support, providing comfort and emotional support, and educating the patient and family. -Continuous assessment of the progressive paralysis associated with GBS is essential to timely intervention and the prevention of respiratory arrest and further neurologic insult. -After the patient is intubated and placed on mechanical ventilation, close observation for pulmonary complications such as atelectasis, pneumonia, and pneumothorax is necessary. -Autonomic dysfunction in the GBS patient can produce variations in heart rate and blood pressure that can reach extreme values. -Hypertension and tachycardia may require beta-blocker therapy.

autonomic dysreflexia

-The return of reflexes after the resolution of spinal shock means patients with an injury level at T6 or higher may develop autonomic hyperrreflexia. -Autonomic hyperreflexia (also known as autonomic dysreflexia) is a massive uncompensated cardiovascular reaction mediated by the sympathetic nervous system. -It involves stimulation of sensory receptors below the level of the SCI. -The intact sympathetic nervous system below the level of the injury responds to the stimulation with a reflex arteriolar vasoconstriction that increases BP, but the parasympathetic nervous system is unable to directly counteract these responses via the injured spinal cord. -Baroreceptors in the carotid sinus and aorta sense the hypertension and stimulate the parasympathetic system. -This results in a decrease in heart rate, but visceral and peripheral vessels do not dilate because efferent impulses cannot pass through the injured spinal cord. -The most common precipitating cause of autonomic hyperrreflexia is a distended bladder or rectum. -However, autonomic hyperreflexia can be caused by any sensory stimulation, including contraction of the bladder or rectum, stimulation of the skin, or stimulation of the pain receptors. Clinical Manifestations: -Hypertension (up to 300 mm Hg systolic) -Throbbing headache -Marked diaphoresis above the level of the injury -Bradycardia (30 to 40 beats/minute). -It is important to measure BP when a patient with a SCI complains of a headache. Nursing Interventions: -Autonomic hyperreflexia is a life-threatening situation that requires immediate resolution. -If resolution does not occur, it can lead to status epilepticus, stroke, myocardial infarction, and even death. -Nursing interventions in this serious emergency include elevating the head of the bed 45 degrees or sitting the patient upright (this lowers ICP to counter HTN), notification of the physician, and assessment to determine the cause. -The most common cause is bladder irritation. -Immediate catheterization to relieve bladder distention may be necessary. -Lidocaine jelly should be instilled in the urethra before catheterization. -If a catheter is already in place, it should be checked for kinks or folds. -If plugged, perform small-volume irrigation slowly and gently to open the catheter, or insert a new catheter. -Stool impaction can also cause autonomic hyperreflexia. -Perform a digital rectal examination (if trained) only after application of an anesthetic ointment to decrease rectal stimulation and to prevent an increase of symptoms. -Remove all skin stimuli, such as constrictive clothing and tight shoes. -Monitor BP frequently during the episode. -If symptoms persist after the source has been relieved, administer a rapid onset and short duration agent such as nitroglycerine, nitroprusside, or hydralazine. -Continue monitoring until the vital signs stabilize. -Teach the patient and caregiver to recognize the causes and symptoms of autonomic hyperreflexia. -They must understand the life-threatening nature of this dysfunction and know how to relieve the cause, and activate the emergency response system (ERS) if needed.

chest tube management

-Once chest tube is placed drainage must be monitored closely ->200 ml/hour of blood from chest tube may need replaced -FOCA for chest tube assessment: •F: fluctuation in the water seal chamber •O: output •C: color of drainage •A: air leak

head injury

-Head injury includes any injury or trauma to the scalp, skull, or brain. -A serious form of head injury is traumatic brain injury (TBI). -Statistics regarding the occurrence of head injuries are incomplete because many victims die at the injury scene or because the condition is considered minor and health care services are not sought. -In the United States in hospital emergency departments, an estimated 1.7 million persons are treated and released with TBI. -Fifty thousand people die and 275,000 persons are hospitalized with TBI. Of individuals hospitalized, 20% of the patients die. -At least 5.3 million Americans (2% of the U.S. population) currently live with disabilities resulting from TBI -TBI are twice as common in males -High potential for poor outcome -The most common causes of head injury are falls and motor vehicle accidents. -Other causes of head injury include firearms, assaults, sports-related trauma, recreational injuries, and war-related injuries -The majority of deaths after a head injury occur immediately after the injury, either from the direct head trauma or from massive hemorrhage and shock. -Deaths occurring within a 2 hours of the trauma are caused by progressive worsening of the brain injury or internal bleeding. -Deaths occurring 3 weeks or more after the injury result from multisystem failure or a venous (slow) bleed. -Expert nursing care in the weeks after the injury is crucial in decreasing the mortality risk and in optimizing patient outcomes. Types of Head Injuries: -Skull fractures frequently occur with head trauma. -There are several ways to describe skull fractures: (1) linear or depressed; (2) simple, comminuted, or compound; and (3) closed or open. -Linear fracture occurs when there is a break in continuity of bone without alteration of relationship of parts. It is associated with low-velocity injuries. -A depressed skull fracture is an inward indentation of skull and is associated with a powerful blow. -A simple linear or depressed skull fracture is without fragmentation or communicating lacerations. It is caused by low to moderate impact. -A comminuted fracture occurs when there are multiple linear fractures with fragmentation of bone into many pieces. It is associated with direct, high-momentum impact. -An example of a compound fracture is a depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity. This is associated with severe head injury. -Fractures may be closed or open, depending on the presence of a scalp laceration or extension of the fracture into the air sinuses or dura. -The location of the fracture determines the clinical manifestations. -The major potential complications of skull fractures are intracranial infections, hematoma, and meningeal and brain tissue damage. -Note that in cases where a basilar skull fracture is suspected, an orogastric tube should be inserted rather than a nasogastric tube. Basilar Skull Fracture: -A basilar skull fracture is a specialized type of linear fracture that occurs when the fracture involves the base of the skull. -Manifestations can evolve over the course of several hours, vary with the location and severity of fracture, and may include cranial nerve deficits, Battle's sign (postauricular ecchymosis), and periorbital ecchymosis (raccoon eyes). -This fracture generally is associated with a tear in the dura and subsequent leakage of CSF. -Rhinorrhea (CSF leakage from the nose) or otorrhea (CSF leakage from the ear) generally confirms that the fracture has traversed the dura. -Rhinorrhea may also manifest as postnasal sinus drainage. The significance of rhinorrhea may be overlooked unless the patient is specifically assessed for this finding. -The risk of meningitis is high with a CSF leak, and antibiotics should be administered to prevent the development of meningitis. -Two methods of testing can be used to determine whether the fluid leaking from the nose or ear is CSF. -The first method is to test the leaking fluid with a Dextrostix or Tes-Tape strip to determine whether glucose is present. -CSF gives a positive reading for glucose. -If blood is present in the fluid, testing for the presence of glucose is unreliable because blood also contains glucose. -In this event, look for the halo or ring sign. To perform this test, allow the leaking fluid to drip onto a white gauze pad (4 × 4) or towel, and then observe the drainage. -Within a few minutes, the blood coalesces into the center, and a yellowish ring encircles the blood if CSF is present. -Note the color, appearance, and amount of leaking fluid because both tests can give false-positive results. -Basilar skull fractures can cause other damage -Brain injuries are categorized as diffuse (generalized) or focal (localized). -In a diffuse injury (e.g., concussion, diffuse axonal), damage to the brain cannot be localized to one particular area of the brain. -In a focal injury (e.g., contusion, hematoma), damage can be localized to a specific area of the brain. -Brain injury can be classified as minor (GCS 13 to 15), moderate (GCS 9 to 12), and severe (GCS 3 to 8) Nursing Assessment: -Past medical history of trauma -Mechanism of injury -Medications history, anticoagulants -Altered mental status -Lacerations, contusions, abrasions -Hematoma -Battles sign -Periorbital edema and ecchymosis -Otorrhea -Exposed brain tissue -Respiratory: •Rhinorrhea, impaired gag reflex, inability to maintain a patent airway •Impending herniation: altered/irregular respiratory rate and pattern -Cardiovascular •Impending herniation: Cushing's triad (systolic hypertension with widening pulse pressure, bradycardia with full and bounding pulse, irregular respirations) -Gastrointestinal: •Vomiting, projectile vomiting, bowel incontinence -Urinary: •Bladder incontinence -Neurological: •Altered LOC, GCS, Seizure, Pupil dysfunction, Cranial nerve Deficits -Musculoskeletal: •Motor deficit /impairment, weakness, palmar drift, paralysis, spasticity, decorticate or decerebrate posturing, muscular rigidity/increased tone, flaccidity, ataxia -Reproductive: •Uninhibited sexual expression -Location and type of hematoma, edema, skull fracture, and/or foreign body on CT scan and/or MRI -Abnormal EEG -Positive toxicology screen or alcohol level -Hyper or hypo blood glucose level -Increased ICP Diagnostic Studies: -CT scan is the best diagnostic test to evaluate for head trauma because it allows rapid diagnosis and intervention in the acute care setting. -MRI, PET, and evoked potential studies may also be used in the diagnosis and differentiation of head injuries. -An MRI scan is more sensitive than the CT scan in detecting small lesions. -Transcranial Doppler studies allow for the measurement of cerebral blood flow (CBF) velocity. -A cervical spine x-ray series, CT scan, or MRI of the spine may also be indicated since cervical spine trauma often occurs at the same time as a head injury. -In general, the diagnostic studies are similar to those used for a patient with increased ICP. -Glasgow Coma Scale Interprofessional Care: -Principles in caring for patients with a head injury include: •Measures to prevent secondary injury by treating cerebral edema and managing increased ICP •Timely diagnosis •Surgery (if necessary). -For the patient with concussion and contusion, observation and management of increased ICP are the primary management strategies. -The treatment of skull fractures is usually conservative. -For depressed fractures and fractures with loose fragments, a craniotomy is necessary to elevate the depressed bone and remove the free fragments. -If large amounts of bone are destroyed, the bone may be removed (craniectomy), and a cranioplasty will be needed at a later time. -In cases of large acute subdural and epidural hematomas, or those associated with significant neurologic impairment, the blood must be removed through surgical evacuation. -A craniotomy is generally performed to visualize and allow control of the bleeding vessels. -Burr-hole openings may be used in an extreme emergency for a more rapid decompression, followed by a craniotomy. -A drain may be placed postoperatively for several days to prevent reaccumulation of blood. -In cases where extreme swelling is expected (e.g., DAI, hemorrhage), a craniectomy may be performed where a piece of the skull is removed to reduce the pressure inside the cranial vault, thus reducing the risk of herniation. Emergency Treatment: -Ensure patent airway. -Stabilize cervical spine. -Administer O2 via non-rebreather mask. -Establish IV access with two large-bore catheters to infuse normal saline or lactated Ringer's solution. -Intubate if GCS <8. -Control external bleeding with sterile pressure dressing. -Remove patient's clothing. -Maintain patient warmth using blankets, warm IV fluids, overhead warming lights, warm humidified O2. -Ongoing monitoring of: •Vital signs, level of consciousness, O2 saturation, cardiac rhythm, Glasgow Coma Scale score, pupil size and reactivity. •Assess for rhinorrhea, otorrhea, scalp wounds. -Anticipate need for intubation if gag reflex is impaired or absent. -Assume neck injury with head injury. -Administer fluids cautiously to prevent fluid overload and increasing ICP. -Poikothermia: client cannot regulate their body temperature, body takes whatever temperature is in their environment Planning: The overall goals are that the patient with an acute head injury will (1) Maintain adequate cerebral oxygenation and perfusion (2) Remain normothermic (3) Achieve control of pain and discomfort (4) Be free from infection (5) Have adequate nutrition; and (6) Attain maximal cognitive, motor, and sensory function. Acute Care: -Management at the injury scene can have a significant impact on the outcome of the head injury. -The general goal of nursing management of the head-injured patient is to maintain cerebral oxygenation and perfusion and prevent secondary cerebral ischemia. -Surveillance or monitoring for changes in neurologic status is critically important because the patient's condition may deteriorate rapidly, necessitating emergency surgery. -Because of the close association between hemodynamic status and cerebral perfusion, be aware of any coexisting injuries or conditions. -Perform neurologic assessments at intervals based on the patient's condition. The GCS is useful in assessing the LOC -Indications of a deteriorating neurologic state, no matter how subtle, such as a decreasing LOC or decreasing motor strength, should be reported to the health care provider. Monitor the patient's condition closely. -Explain the need for frequent neurologic assessments to both the patient and caregiver. -Behavioral manifestations associated with head injury can result in a frightened, disoriented patient who is combative and resists help. -Your approach should be calm and gentle. -A family member may be available to stay with the patient and thus prevent increasing anxiety and fear. -One of the most important needs for the caregiver and family members in the acute injury phase is information about the patient's diagnosis, treatment plan, and rationale for the interventions. -The major focus of nursing care for the brain-injured patient relates to increased ICP. -However, there may be problems that require specific nursing interventions. -Eye problems may include loss of the corneal reflex, periorbital ecchymosis and edema, and diplopia. -Loss of the corneal reflex may necessitate administering lubricating eye drops or taping the eyes shut to prevent abrasion. -Periorbital ecchymosis and edema decrease with time, but cold and, later, warm compresses provide comfort and hasten the process. -Diplopia can be relieved by use of an eye patch. A consult with an ophthalmologist should be considered. -Hyperthermia may occur from injury to or inflammation of the hypothalamus. -Elevations in body temperature can result in increased CBF, cerebral blood volume, and ICP. -Increased metabolism secondary to hyperthermia increases metabolic waste, which in turn produces further cerebral vasodilation. -Avoid hyperthermia with a goal of 36°to 37°C as the standard of care. -Use interventions to reduce temperature in conjunction with sedation as necessary to prevent shivering. -If CSF rhinorrhea or otorrhea occurs, inform the HCP immediately. -The head of the bed may be raised to decrease the CSF pressure so that a tear can seal. -A loose collection pad may be placed under the nose or over the ear. Do not place a dressing in the nasal or ear cavities and document the amount of drainage each shift. -Instruct the patient not to sneeze or blow the nose. -Do not use nasogastric tubes. •Do not perform nasotracheal suctioning on these patients because of the high risk of meningitis. -Nursing measures specific to the care of the immobilized patient, such as those related to bladder and bowel function, skin care, and infection, are also indicated. -Nausea and vomiting may be a problem and can be alleviated by antiemetic drugs. -Headache can usually be controlled with acetaminophen or small doses of codeine. -If the patient's condition deteriorates, intracranial surgery may be necessary. -A burr-hole opening or craniotomy may be indicated, depending on the underlying injury that is causing the problems. -The emergency nature of the surgery may hasten the usual preoperative preparation. -Consult with the neurosurgeon to determine specific preoperative nursing measures. -The patient is often unconscious before surgery, making it necessary for a family member to sign the consent form for surgery. -This is a difficult and frightening time for the patient's caregiver and family and requires sensitive nursing management. -The suddenness of the situation makes it especially difficult for the family to cope. -Use the interprofessional team, including social workers, to assist the patient and family throughout the hospitalization and recovery time. Ambulatory Care: -Once the condition has stabilized, the patient is usually transferred for acute rehabilitation management. -There may be chronic problems related to motor and sensory deficits, communication, memory, and intellectual functioning. Many of the principles of nursing management of the patient with a stroke are appropriate for these patients. -Conditions that may require nursing and interprofessional management include poor nutritional status, bowel and bladder management, spasticity, dysphagia, deep vein thrombosis, and hydrocephalus. -The patient's outward appearance is not a good indicator of how well the patient will ultimately function in the home or work environment. -The outward physical appearance does not necessarily reflect what has happened in the brain. -Seizure disorders may occur in patients with nonpenetrating head injury. -Seizures may develop during the first week after the head injury. -Some patients may not develop a seizure disorder until years after the initial injury. -Antiseizure drugs may be used prophylactically to manage posttraumatic seizure activity, but this practice is controversial as previously discussed. -The mental and emotional sequelae of brain trauma are often the most incapacitating problems. -One of the consequences of TBI is that the person may not realize that a brain injury has occurred. -Many of the patients with head injuries who have been comatose for more than 6 hours undergo some personality change. -They may suffer loss of concentration and memory and defective memory processing. -Personal drive may decrease. Apathy may increase. Euphoria and mood swings, along with a seeming lack of awareness of the seriousness of the injury, may occur. -The patient's behavior may indicate a loss of social restraint, judgment, tact, and emotional control. -Progressive recovery may continue for years. -Specific nursing management in the posttraumatic phase depends on specific residual deficits. -Being able to return to work and maintaining employment is one of the challenges during the recovery period. -In all cases, the family must be given special consideration. -They need to understand what is happening and be taught appropriate interaction patterns. -Provide guidance and referrals for financial aid, child care, and other personal needs. -Assist the family in involving the patient in family activities whenever possible. -Help the patient and family remain hopeful. The family often has unrealistic expectations of the patient as the coma begins to recede. -The family expects full return to pretrauma status. -In reality, the patient usually experiences a reduced awareness and ability to interpret environmental stimuli. -Prepare the family for the patient's emergence from coma and explain that the process of awakening often takes several weeks. -In addition, arrange for social work and chaplain consultations for the family. -When it is the time for discharge planning, the patient, caregiver, and family may benefit from specific posthospitalization instructions to avoid family-patient friction. -Special "no" policies that may be appropriately suggested by the neurosurgeon, neuropsychologist,e and nurse include no drinking of alcoholic beverages, no driving, no use of firearms, no working with hazardous implements and machinery, and no unsupervised smoking. -Family members, particularly spouses, go through role transition as the role changes from that of spouse to that of caregiver. Health Promotion - Secondary Prevention: -One of the best ways to prevent head injuries is to prevent car and motorcycle accidents. -The use of helmets by cyclists has led to fewer TBIs. -The use of car seat belts and the use of child car seats are also associated with reduced TBI mortality rates. -Be active in campaigns that promote driving safety and speak to driver education classes regarding the dangers of unsafe driving and of driving after drinking alcohol and using drugs. -The use of seat belts in cars and the use of helmets for riding on motorcycles are the most effective measures for increasing survival after crashes. -Protective helmets should also be worn by lumberjacks, construction workers, athletes who play contact sports, miners, horseback riders, bicycle riders, snowboarders, skiers, and skydivers. -Additionally, individuals who are at risk for falls (e.g., older adults) should be evaluated for safety in the home, as falls are the second leading cause of head injuries.

intervertebral disc disease

-Intervertebral discs separate the vertebrae of the spinal column and help absorb shock for the spine. -An intervertebral disc disease involves the deterioration, herniation, or other dysfunction of the intervertebral discs. -Disc disorders can affect the cervical, thoracic, and lumbar spine. -Degenerative disc disease (DDD) results from increased wear and tear on the intervertebral discs with aging. -The discs lose their elasticity, flexibility, and shock-absorbing abilities. Unless it is accompanied by pain, this wear and tear condition is a normal process. -Thinning of the discs occurs as the nucleus pulposus (gelatinous center of the disc) starts to dry out and shrink. -This limits the disc's ability to distribute pressure loads between the vertebrae. -The pressure is then transferred to the annulus fibrosus (strong outside portion of the disc), causing progressive destruction. -When the disc is damaged, the nucleus pulposus may seep through a torn or stretched annulus. -This is called a herniated disc (slipped disc), a condition in which a spinal disc bulges outward between the vertebrae. -The spinal nerves emerge from the spinal column through an opening (intervertebral foramen) between adjacent vertebrae. -Herniated discs can press against these nerves ("pinched nerve") causing radiculopathy (radiating pain, numbness, tingling, and diminished strength and/or range of motion). -Osteoarthritis of the spine is associated with DDD as the stresses placed on the vertebrae can result in osteoarthritis. -As the poorly lubricated joints rub against each other, the protective cartilage is damaged and painful bone spurs occur as one of changes found in osteoarthritis. Clinical Manifestations: -In lumbar disc disease the most common manifestation is low back pain. -Radicular pain that radiates down the buttock and below the knee, along the distribution of the sciatic nerve, generally indicates disc herniation. -A positive straight leg raising test may indicate nerve root irritation. -Back or leg pain may be reproduced by raising the leg and flexing the foot at 90 degrees. -Low back pain from other causes may not be accompanied by leg pain. -Reflexes may be depressed or absent unilaterally or bilaterally, depending on the spinal nerve root involved. -Paresthesia or muscle weakness in the legs, feet, or toes may occur. -Muscle weakness: muscle atrophy -Compare extremities: grips and pushes, circumference Multiple Nerve Root Compression: -Multiple nerve root compressions (cauda equina syndrome) from a herniated disc, tumor, or epidural abscess may be marked by (1) severe low back pain, (2) progressive weakness, (3) increased pain, and (4) bowel and bladder incontinence. -This condition is a medical emergency that requires surgical decompression to reduce pressure on the nerves and prevent permanent loss of function -Alert the provider immediately! Cervical Disc Disease: -In cervical disc disease pain radiates into the arms and hands, following the pattern of the involved nerve. -Similar to lumbar disc disease, reflexes may or may not be present. -The handgrip is often weak. -Because manifestations of cervical disc disease may include shoulder pain and dysfunction, the HCP must rule out shoulder disorders as part of the diagnosis. -Report change in baseline immediately with nerve involvement Diagnostic Studies: -X-rays are done to detect any structural defects. -A myelogram, MRI, or CT scan is helpful in localizing the damaged site. -An epidural venogram or discogram may be needed if other diagnostic studies are inconclusive. -An EMG of the extremities can be performed to determine the severity of nerve irritation or to rule out other conditions such as peripheral neuropathy. Interprofessional Care: -The patient with suspected disc damage is usually managed with conservative therapy. -Limitation of movement (brace, corset, or both) -Local heat or ice -Ultrasound and massage -Skin traction -Transcutaneous electrical nerve stimulation (TENS) -Drug therapy: •NSAIDs •Short-term corticosteroids •Opioids •Muscle relaxants •Antiseizure drugs, antidepressants -Epidural corticosteroid injections -When symptoms subside, the patient should begin back strengthening exercises twice a day and continue for life. -Teach the patient the principles of good body mechanics. -Discourage extremes of flexion and torsion. -With a conservative treatment plan, most patients heal in 6 months. Surgical Therapy: -If conservative treatment is unsuccessful, radiculopathy becomes worse, or loss of bowel or bladder control (cauda equine syndrome) occurs, surgery may then be considered. -Surgery for a damaged disc is generally indicated when the patient is in constant pain and/or has a persistent neurologic deficit. -An intradiscal electrothermoplasty (IDET) is a minimally invasive outpatient procedure for treatment of back and sciatica pain. •A needle is inserted into the affected disc with x-ray guidance. •A wire is then threaded down through the needle and into the disc. •As the wire is heated, the small nerve fibers that have invaded the degenerating disc are destroyed. •The heat also partially melts the annulus fibrosus. •This causes the body to generate new reinforcing proteins in the fibers of the annulus. -Another outpatient technique is radiofrequency discal nucleoplasty (coblation nucleoplasty). •A needle is inserted into the disc similar to IDET. •Instead of a heated wire, a special radiofrequency probe is used. •The probe generates energy that breaks up the molecular bonds of the gel in the nucleus pulposus. •Up to 20% of the nucleus is removed. •This decompresses the disc and reduces pressure on the disc and the surrounding nerve roots. •Subsequent pain relief varies among patients. -A third procedure involves use of an interspinous process decompression system (X Stop). •This titanium device fits onto a mount that is placed on vertebrae in the lower back. •The X Stop is used in patients with pain due to lumbar spinal stenosis. •The device works by lifting the vertebrae off the pinched nerve. -Laminectomy is a common, traditional surgical procedure for lumbar disc disease. •It involves the surgical excision of part of the vertebra (referred to as the lamina) to access and remove the protruding disc. •A third procedure involves use of an interspinous process decompression system (X Stop). •This titanium device fits onto a mount that is placed on vertebrae in the lower back. •The X Stop is used in patients with pain due to lumbar spinal stenosis. •The device works by lifting the vertebrae off the pinched nerve. •Laminectomy is a common, traditional surgical procedure for lumbar disc disease. •It involves the surgical excision of part of the vertebra (referred to as the lamina) to access and remove the protruding disc. •A hospital stay is typical after the procedure. -Diskectomy can also be performed to decompress the nerve root. •Microsurgical diskectomy is a version of the standard procedure. •The surgeon uses a microscope for better visualization of the disc and disc space to aid in the removal of the damaged portion. •This helps to maintain the bony stability of the spine. •Percutaneous diskectomy is a safe and effective outpatient surgical procedure. •A tube is passed through the retroperitoneal soft tissues to the disc with the aid of fluoroscopy. •A laser is then used on the damaged portion of the disc. •Minimal blood loss occurs because of access through small stab wounds. •The procedure decreases rehabilitation time. -The goals of artificial disc replacement surgery are to restore movement and eliminate pain. •The Charité or prodisc-L disc is used in patients with lumbar disc disease associated with DDD. •This artificial disc has a high-density core sandwiched between two cobalt-chromium endplates •Prestige cervical disc system •After the damaged disc is removed, this device is surgically placed in the spine (usually through a small incision below the umbilicus) after the damaged disc is removed. •The disc restores movement at the level of the implant. •The Prodisc-L is another type of artificial lumbar disc that can be used to treat DDD. •Options for treatment of DDD of the cervical spine include the Prestige cervical disc, Mobi-C disc, and Secure-C artificial cervical disc. -A spinal fusion may be needed if the spine is unstable. •The spine is stabilized by creating ankylosis (fusion) of adjacent vertebrae with a bone graft from the patient's fibula or iliac crest (autograft) or from a donated cadaver bone (allograft). •Metal fixation with rods, plates, or screws may be placed at the time of spinal surgery to provide more stability and decrease vertebral motion. •A posterior lumbar fusion may be performed in patients to provide extra support for bone grafting or a prosthetic device. •Bone morphogenetic protein (BMP), a genetically engineered protein, may be used to stimulate bone growth of the graft in spinal fusions. •A dissolvable sponge soaked with BMP is implanted into the spine. •The protein on the sponge stimulates the body's cells to become active and produce bone. •BMP begins the process of fusion, which continues even after the protein and sponge dissolve to leave living bone behind. Nursing Management: -After vertebral disc surgery, postoperative nursing interventions mainly focus on maintaining proper alignment of the spine until healing has occurred. -Depending on the type and extent of surgery and the surgeon's preference, the patient may be able to dangle the legs at the side of the bed, stand, or even ambulate the day of surgery. -After lumbar fusion, place pillows under the patient's thighs when supine and between the legs when in the side-lying position to provide comfort and ensure alignment. -The patient often fears turning or any movement that may increase pain by stressing the surgical area. -Reassure the patient that proper technique is being used to maintain body alignment. -Enough staff should be available to move the patient without undue pain or strain for the patient or staff. Postoperative Management: -Postoperatively, most patients will require opioids such as morphine IV for 24 to 48 hours. -Patient-controlled analgesia (PCA) allows maintenance of optimal analgesic levels and is the preferred method of continuous pain management during this time. -Once the patient receives oral fluids, oral drugs such as acetaminophen with codeine, hydrocodone (Vicodin), or oxycodone (Percocet) may be used. -Diazepam (Valium) may be prescribed for muscle relaxation. -Assess and document pain intensity and pain management effectiveness -Because the spinal canal may be entered during surgery, cerebrospinal fluid (CSF) leakage is possible. •Immediately report leakage of CSF on the dressing or if the patient complains of severe headache. •CSF appears as clear or slightly yellow drainage on the dressing. •It has a high glucose concentration and will be positive for glucose when tested with a dipstick. •Note the amount, color, and characteristics of drainage. -Frequently assess the patient's peripheral neurologic condition after spinal surgery (every 2 to 4 hours during first 48 hours post surgery). -Movement of the arms and legs and assessment of sensation should at least equal the preoperative status. -Paresthesias (numbness and tingling) may not be relieved immediately after surgery. -Report any new muscle weakness or paresthesias immediately to the surgeon and document this finding in the patient's medical record. -Assess extremity circulation using skin temperature, capillary refill, and pulses. -Report changes from baseline or status immediately -Paralytic ileus and interference with bowel function may occur for several days and may manifest as nausea, abdominal distention, and constipation. -Opioids can also slow bowel elimination. -Assess if the patient is passing gas, has bowel sounds in all quadrants, and has a flat, soft abdomen. -Stool softeners (e.g., docusate [Colace]) and laxatives may prevent and relieve constipation. -Emptying the bladder may be difficult due to activity restrictions, opioids, or anesthesia. -Encourage men to dangle the legs over the side of the bed or stand to urinate if allowed by the surgeon. -Urge patients to use a bedside commode or ambulate to the bathroom when allowed to promote bladder emptying. -Ensure that privacy is maintained. -Intermittent catheterization or an indwelling urinary catheter may be needed by patients who have difficulty urinating. -Loss of sphincter tone or bladder tone may indicate nerve damage. -Monitor for incontinence or difficulty with bowel or bladder elimination, and immediately report problems to the surgeon. -Notify surgeon of decreased sensation in the perineal area -In addition to nursing care appropriate for a patient who had a laminectomy, other nursing activities are indicated if the patient has also had a spinal fusion. -Because a bone graft is usually involved, the postoperative healing time is prolonged compared with a laminectomy. -Activity limitations may be needed for an extended time. -A rigid orthosis (thoracic-lumbar-sacral orthosis or chairback brace) is often used during this period. -Some surgeons want patients to be taught to apply and remove the brace by logrolling in bed. -Others allow their patients to apply the brace in a sitting or standing position. -Verify the surgeon's preferred method before starting this activity. -If surgery is done on the cervical spine, be alert for indications of spinal cord edema such as respiratory distress and a worsening neurologic status of the upper extremities. -After surgery, the patient's neck may be immobilized in a soft or hard cervical collar. -In addition to the primary surgical site, regularly assess the bone graft donor site. -The posterior iliac crest is the most commonly used donor site, although the fibula may also be used. -The donor site usually causes greater pain than the spinal fusion area. -The donor site is bandaged with a pressure dressing to prevent excessive bleeding. -If the donor site is the fibula, frequent neurovascular assessments of the extremity is a postoperative nursing responsibility. -Important to watch for compartment syndrome Teaching Regarding Activity: -Following spinal fusion the patient may experience some immobility of the spine at the fusion site. -Instruct the patient to use proper body mechanics. -Instruct the patient to avoid sitting or standing for prolonged periods. -Encourage activities that include walking, lying down, and shifting weight from one foot to the other when standing. -Instruct the patient on any lifting restrictions after spinal surgery. -Encourage the patient to think through an activity before starting any potentially injurious task such as bending or stooping. -Any twisting movement of the spine is contraindicated. -Teach the patient to use the thighs and knees, rather than the back, should be used to absorb the shock of activity and movement. -A firm mattress or bed board is essential.

thoracic trauma

-25% of motor vehicle crash deaths are related to thoracic trauma -Approximately tens of thousands of deaths per year -Second only to brain and spinal cord injuries as the leading cause of traumatic death -Motor vehicle crashes and interpersonal violence are the two main causes of thoracic trauma -Most thoracic traumas will also involve the abdominal cavity: •Second largest hollow space of the body •Contains the heart, lungs, diaphragm, great vessels, esophagus, ribs, vertebral column, and various muscles •Epicenter of all circulatory and oxygen flow for the body Ruptured Diaphragm: -Dyspnea/ abdominal pain -More common on the left side -Abdominal organs move into thoracic cavity causing respiratory compromise -Decreased breath sounds -Bowel sounds in the lungs -Kehr's Sign: should pair related to blood in the peritoneal cavity -Bowels going into the lungs and heart due to a ruptured diaphragm can cause massive infection

lower extremity immobilization

-After the application of a lower extremity cast or dressing, the extremity should be elevated on pillows above heart level for the first 24 hours. -After the initial phase, a casted extremity should not be placed in a dependent position because of the possibility of excessive edema. -After cast application, observe for signs of compartment syndrome and increased pressure, especially in the heel, anterior tibia, head of fibula, and malleoli. -This increased pressure is manifested by pain or burning in these areas. -Prefabricated knee and ankle splints and immobilizers are used in many settings. -This type of immobilization is easy to apply and remove, which permits close observation of the affected joint for signs of swelling and skin breakdown. -Depending on the injury, removal of the splint or immobilizer facilitates ROM of the affected joint and faster return to function.

acute low back pain

-Low back pain is common and has affected about 80% of adults in the United States at least once during their lives. -Backache is second only to headache as the most common pain complaint. -Low back pain is the leading cause of job-related disability, and a major contributor to missed work days. -Most concern about cervical spinal injuries Etiology and Pathophysiology: -Low back pain is most often due to a musculoskeletal problem. -It may be experienced as localized or diffuse. -In localized pain patients will feel soreness or discomfort when a specific area of the lower back is palpated or pressed. -Diffuse pain occurs over a larger area and comes from deep tissue layers. -Low back pain may be radicular or referred. -Radicular pain is caused by irritation of a nerve root. -Radicular pain is not typically isolated to a single location, but instead radiates or moves along a nerve distribution. -Sciatica is an example of radicular pain. -Referred pain is "felt" or perceived in the lower back, but the source of the pain is another location (e.g., kidneys, lower abdomen). -Low back pain is a common problem because the lumbar region (1) bears most of the weight of the body, (2) is the most flexible region of the spinal column, (3) contains nerve roots that are at risk for injury or disease, and (4) has a naturally poor biomechanical structure. Risk Factors: -Lack of muscle tone -Excess body weight -Pregnancy -Stress -Poor posture -Cigarette smoking -Prior compression fractures of the spine -Congenital spinal problems -Family history of back pain -Jobs that require repetitive heavy lifting, vibration (such as a jackhammer operator), and extended periods of sitting are also associated with low back pain. -Health care personnel who perform direct patient care activities are at high risk for the development of low back pain. -Lifting and moving patients, excessive bending or leaning position, and frequent twisting can result in low back pain that causes lost time and productivity and/or disability. -The causes of low back pain of musculoskeletal origin include (1) acute lumbosacral strain, (2) instability of the lumbosacral bony mechanism, (3) osteoarthritis of the lumbosacral vertebrae, (4) degenerative disc disease, and (5) herniation of an intervertebral disc. -Few definitive diagnostic abnormalities are present with nerve irritation and muscle strain. -One test is the straight leg raising test: positive for disc herniation when radicular pain occurs. •MRI and CT scans are generally not done unless trauma or systemic disease (e.g., cancer, spinal infection) is suspected. -MRI findings may also be limited in the acute phase of an injury due to increased edema near the injury. -Acute low back pain is low back pain that lasts 4 weeks or less. -Most acute low back pain is caused by trauma or an activity that produces undue stress (often hyperflexion) on the lower back. -Examples of trauma or activity that could cause acute back pain are heavy lifting, overuse of the back muscles during yard work, a sports injury, or a sudden jolt in a motor vehicle crash. -Often symptoms do not appear at the time of injury but develop later (usually within 24 hours) because of a gradual increase in pressure on the nerve from an intervertebral disc and/or associated edema. -Symptoms may range from muscle ache to shooting or stabbing pain, limited flexibility and/or range of motion, or an inability to stand upright. Obtain the following important health information from the patient: -Past health history: acute or chronic lumbosacral strain/trauma, osteoarthritis, degenerative disc disease, obesity -Medications: use of opioid analgesics, nonsteroidal anti-inflammatory drugs, muscle relaxants, corticosteroids, over-the-counter remedies (e.g., topical ointments, patches) -Surgery or other treatments: previous back surgery, epidural corticosteroid injections Obtain the following important health information related to pertinent functional health patterns: -Health perception-health management: smoking, lack of exercise -Nutritional-metabolic: obesity -Activity-exercise: poor posture, muscle spasms, activity intolerance -Elimination: constipation Obtain the following important health information related to pertinent functional health patterns: -Sleep-rest: interrupted sleep -Cognitive-perceptual: pain in back, buttocks, or leg associated with walking, turning, straining, coughing, leg raising. Numbness or tingling of legs, feet, toes -Role-relationship: occupations requiring heavy lifting, vibrations, or extended driving; change in role within family structure due to inability to work and provide income Focused assessment findings include the following: -General: •Guarded movement -Neurologic: •Depressed or absent Achilles tendon reflex or patellar tendon reflex •Positive straight leg-raising test, positive crossover straight leg-raising test, positive Trendelenburg test -Musculoskeletal: •Tense, tight paravertebral muscles on palpation, ↓ range of motion in spine -Possible Diagnostic Findings: •Localization of site of lesion or disorder on myelogram, CT scan, or MRI •Determination of nerve root impingement on electromyography (EMG) Nursing Diagnosis: -Acute pain related to muscle spasm and ineffective comfort measures -Impaired physical mobility related to pain as evidenced by movement restrictions and muscle spasms -Ineffective coping related to effects of acute pain -Ineffective health management related to knowledge deficit, complexity of therapeutic regimen, or lack of perceived benefits regarding posture, exercises, and body mechanics The overall goals are that the patient with acute low back pain will: -Report satisfactory pain relief with pain <4 on 10-point scale. -Demonstrate return to prior level of mobility within prescribed restrictions. -Demonstrate correct performance of exercises. -Uses coping behaviors effectively to adapt to effects of acute pain. -Integrate a program of appropriate posture, body mechanics, exercises, and weight management into daily routine. Health Promotion: -Use proper body mechanics at all times to serve as a role model. -This includes increasing the patient's bed height, bending at the knees, asking for help in lifting and moving patients, and using lifting devices. -Assess the patient's use of body mechanics and offer advice when the person does activities that could produce back strain. -Some HCPs refer patients with back pain to a program called "Back School." •This is formal program usually taught by health professionals such as HCPs, nurses, and physical therapists. •It is designed to teach the patient how to minimize back pain and avoid repeat episodes of low back pain. -Referral to a physical therapist or personal trainer to address posture as well as core and abdomen strength may also be appropriate. -Recommend flat shoes or shoes with low heels and shock-absorbing shoe inserts for women. -Advise patients to maintain healthy body weight. Excess body weight places additional stress on the lower back and weakens the abdominal muscles that support the lower back. -The position assumed while sleeping is also important in preventing low back pain. •Advise patients to avoid sleeping in a prone position because it produces excessive lumbar lordosis, placing excessive stress on the lower back. •A firm mattress is recommended. Encourage the patient to sleep in a supine or side-lying position with the knees and hips flexed to prevent unnecessary pressure on support muscles, ligaments, and lumbosacral joints. •Can put a pillow between the knees -Teach patients the importance of smoking cessation. Tobacco use impairs circulation to the intervertebral discs and may contribute to low back pain. -Bulging disc is acute: want to stretch people out -Herniated disc: put in skin traction so disc is not compressed all the time Acute Care: -Treat as outpatient if not severe: •NSAIDs, muscle relaxants (cyclobenzaprine [Flexeril]) •Massage •Back manipulation •Acupuncture •Cold and hot compresses -Severe pain: •Corticosteroids •Opioids-IV, PO, PCA, patches, long acting, short acting •Opiate Naïve •Non-Opiate Naïve Patient Teaching: -Teach patients the cause of their pain, ways to prevent additional episodes, and strengthening and stretching exercises -Although exercises are often taught by a physical therapist, reinforce the type and frequency of prescribed exercise and the rationale for the program. -Sleep in a side-lying position with knees and hips bent -Sleep on back with a lift under knees and legs or back with 10-inch-high pillow under knees to flex hips and knees -If patients have to sleep on their back, put a pillow between their knees -Prevent lower back from straining forward by placing a foot on a step or stool during prolonged standing -Maintain appropriate body weight -Begin exercises with 2- or 3-minute warm-up period by moving arms and legs, alternate relaxing and tightening muscles; exercise slowly with smooth movements. -Exercise 15 minutes in the morning and evening regularly -Carry light items close to body -Use local heat and cold application -Use a lumbar roll or pillow for sitting -Do NOT: •Lean forward without bending knees •Lift anything above level of elbows •Stand in one position for prolonged time •Sleep on abdomen or on back or side with legs out straight •Exercise without consulting health care provider if having severe pain

heat stroke

-Most serious form of heat stress -Failure of hypothalamic thermoregulatory processes -Medical emergency: vasodilation, ↑ sweating and respiratory rate deplete fluids and electrolytes, specifically sodium -Death is related to amount of time patient's body temperature remains elevated -Prognosis is related to: •Age •Baseline health status •Length of exposure Clinical Manifestations: -Eventually, sweat glands stop functioning, and core temperature increases rapidly, within 10 to 15 minutes. -The patient has a core temperature greater than 105.8° F (41° C), altered mental status, absence of perspiration, and circulatory collapse. -The skin is hot, dry, and ashen. -A range of neurologic symptoms occur (e.g., hallucinations, loss of muscle coordination, combativeness) because the brain is extremely sensitive to thermal injuries. -Cerebral edema and hemorrhage may occur as a result of direct thermal injury to the brain and decreased cerebral blood flow. -When sweat glands stop functioning, homeostasis has stopped, and the patient is trying to die -Often, interosseous injections are necessary Interprofessional Care: -Give 100% O2 to compensate for the patient's hypermetabolic state. -Ventilation with a BVM or intubation and mechanical ventilation may be required. -Correct fluid and electrolyte imbalances and start continuous ECG monitoring for dysrhythmias. -Various cooling methods are available. These include removing clothing, covering with wet sheets, and placing the patient in front of a large fan (evaporative cooling); immersing the patient in a cool water bath (conductive cooling); applying ice packs to the groins and axilla; and, in refractory cases, peritoneal lavaging with iced fluids. -Whatever method is selected, closely monitor the patient's temperature and control shivering. -Shivering increases core temperature due to the heat generated by muscle activity. -This complicates cooling efforts. -Give chlorpromazine (Thorazine) IV to control shivering. -Antipyretics are not effective in this situation because the elevated temperature is not related to infection. -Monitor for signs of Rhabdomyolysis: •Skeletal muscle breakdown, urine that is red/rusty in color -Myoglobinuria •Kidneys at risk for injury -Disseminated intravascular coagulation (DIC): obtain clotting studies -Teaching focuses on prevention

amyotrophic lateral sclerosis (ALS)

-Also called Lou Gehrig's disease -Progressive loss of motor neurons -Intact cognition -Muscle wasting -Loss of muscle function -Progressive respiratory insufficiency-mechanical ventilation -2-5 year life expectancy -Steven Hawking: 50 years with ALS -Men 50-70 years of age have a higher incidence -Scarring of motor pathways -Stops innervation of the muscle -Progressive muscle wasting Clinical Manifestations: -Early: •Tripping, weak hand grips, speech, swallowing •Pain, spasticity: fasciculations, drooling, constipation, GERD •Falls, injury -Late: •Aspiration •Respiratory failure •Supportive care from immobility •Advance directives Nursing Diagnosis Priorities: -Reducing aspiration/risk -Communication facilitation -Respiratory monitoring/effort/effectiveness -Pain management from MSK -Fall risk reduction -Diversional activities and support cognitive function

amputation

-Removal of an extremity by trauma or surgery -Goal of surgery: preserve the greatest extremity length and function while removing all infected, pathologic, or ischemic tissue. -Goals of nursing care: pain management, maximum rehabilitation potential, ability to cope with body image changes Indications for Amputation: -Circulatory impairment from PVD -Traumatic or thermal injury -Osteomyelitis -Malignant tumors -Extremity infection -Aging Adults: highest incidence of amputation for treatment of PVD, atherosclerosis, or diabetes -Assessment and stabilization are priority: mechanism of injury, blood loss, shock Post Op: -Watch for hemorrhaging -Blood loss -Phantom pain -Compression bandage -Tourniquet if life threatening Amputation Considerations: -Level of amputation -Preservation of function -Weight bearing ability of the stump -Prosthetic fitting

burn injuries and smoke inhalation

-Thermal burns -Chemical burns -Electrical burns -Cold thermal injury -Smoke inhalation injuries Smoke Inhalation Injuries: -Smoke and inhalation injuries from breathing noxious chemicals or hot air can cause damage to the tissues of the respiratory tract. -Redness and airway edema may result. -Smoke inhalation injuries are a major predictor of mortality in burn patients. -Rapid initial and ongoing assessment is critical. -Assess for signs and symptoms of airway compromise and pulmonary edema that can develop over the first 12-48 hours. -Three types: metabolic asphyxiation, upper airway injury, lower airway injury Metabolic Asphyxiation: -Carbon monoxide (CO) poisoning -CO is produced by incomplete combustion of burning materials -Inhaled CO displaces oxygen: •Hypoxia •Carboxyhemoglobinemia •Death -The majority of deaths at a fire scene are the result of inhaling certain smoke elements, primarily carbon monoxide (CO), or hydrogen cyanide. -Hypoxia and ultimately death when CO levels are 20% or greater -Treat with 100% humidified oxygen -CO poisoning may occur in absence of burn injury to skin Upper Airway Injury: -Injury to mouth, oropharynx, and/or larynx -Thermally produced -Hot air, steam, or smoke -Swelling may be massive and onset rapid -Eschar and edema may compromise breathing -Swelling from scald burns can be lethal -Mucosal burns of the oropharynx and larynx are manifested by redness, blistering, and edema -Mechanical obstruction can occur quickly, presenting a true airway emergency -Reliable clues to this injury: •Presence of facial burns •Singed nasal hair •Hoarseness, painful swallowing •Darkened oral and nasal membranes •Carbonaceous sputum •History of being burned in enclosed space •Clothing burns around neck and chest Lower Airway Injury: -Injury to trachea, bronchioles, and alveoli -Injury is related to length of exposure to smoke or toxic fumes -Pulmonary edema may not appear until 12 to 48 hours after burn •Manifests as acute respiratory distress syndrome (ARDS) Location of Burn: -Burns to the face and neck and circumferential burns to the chest/back may interfere with breathing as a result of mechanical or respiratory obstruction secondary to edema or leathery, devitalized burn tissue (eschar). •These burns may also signal the possibility of smoke or inhalation injury. -Burns to the hands, feet, joints, and eyes are of concern because they make self-care very difficult and may jeopardize future function. •Burns to the hands and feet are challenging to manage because of superficial vascular and nerve supply systems that need to be protected while the burn wounds are healing. -Burns to the ears and the nose are at risk for infection as the skin is very thin and the underlying skeleton is frequently exposed. -Burns to the buttocks or perineum are at high risk for infection from urine or feces contamination. Patient Risk Factors: -Any patient with preexisting heart, lung, or kidney disease has a poorer prognosis for recovery because of the increased demands placed on the body by a burn injury. -The patient with diabetes mellitus or peripheral vascular disease is at high risk for poor healing and gangrene, especially with foot and leg burns. -Physical weakness renders patient less able to recover: •Alcoholism •Drug abuse •Malnutrition -Concurrent fractures, head injuries, or other trauma leads to a more difficult time recovering Prehospital Phase (Inhalation Injury): -Watch for signs of respiratory distress -Treat quickly and efficiently if they are to survive -Use special SpCO oximetry (normal SpO2 is unreliable) -100% humidified oxygen if CO poisoning is suspected: continue until carboxyhemoglobin levels return to normal -Patients with both body burns and inhalation injury must be transferred to the nearest burn center. Emergent Phase Complications: -Respiratory system: •Upper airway burns: edema formation, mechanical airway obstruction and asphyxia -Lower airway injury: impaired gas exchange -Respiratory failure due to: •Pneumonia •Pulmonary edema -Upper airway distress may occur with or without smoke inhalation, and airway injury at either level may occur in the absence of burn injury to the skin. -The patient may need a fiberoptic bronchoscopy and carboxyhemoglobin blood levels to confirm a suspected inhalation injury. -Look in the prehospital and ED notes to see if the patient was exposed to smoke or fumes. -Examine any sputum that the patient may produce for any carbon. -Watch for signs of impending respiratory distress, such as increased agitation, anxiety, restlessness, or a change in the rate or character of the patient's breathing as symptoms may not be present immediately. -The patient with preexisting respiratory problems is more likely to develop a respiratory infection. -Pneumonia is a common complication of major burns and the leading cause of death in patients with an inhalation injury. Emergent Phase Nursing/ Interprofessional Management: -Depending on the acuity of the patient, the duration of time spent in each phase varies greatly, and conditions improve and worsen unpredictably on an almost daily basis. Care changes accordingly. -Although physiotherapy and occupational therapy are a focus of the acute and rehabilitative phases, proper positioning and splinting begin at the time of admission. -Airway management frequently involves early endotracheal (preferably orotracheal) intubation. -Early intubation removes the need for emergency tracheostomy after respiratory problems have become apparent. -In general, the patient with major injuries involving burns to the face and neck requires intubation within 1 to 2 hours after burn injury. -PEEP to prevent atelectasis -After intubation, the patient is placed on ventilatory support, and the delivered oxygen concentration is based on ABG values. -Extubation may be indicated when the edema resolves, usually 3 to 6 days after burn injury, unless severe inhalation injury exists. -Escharotomies of the chest wall may be needed to relieve respiratory distress secondary to circumferential, full-thickness burns of the neck and chest. -Within 6 to 12 hours after injury in which smoke inhalation is suspected, a fiberoptic bronchoscopy should be performed to assess the lower airway. -When intubation is not done, treatment of inhalation injury includes administration of 100% humidified O2 as needed. -Place the patient in a high Fowler's position, unless contraindicated (e.g., spinal injury), and encourage coughing and deep breathing every hour. -Reposition the patient every 1 to 2 hours, and provide chest physiotherapy and suctioning as ordered. -If severe respiratory distress develops, intubation and mechanical ventilation are started. -Continue to assess oxygen needs -Continue to monitor respiratory status -Non-intubated clients: •High Fowler's position •Coughing and deep breathing every hour •Reposition the patient every 1 to 2 hours •Chest physiotherapy and suctioning as ordered -Monitor for signs of complications (pneumonia) -Safety Alert: patient with CO (carbon monoxide) poisoning will have normal SPO2 in spite of elevated CO levels. Use of SPCO monitor needed

trauma

-Trauma is defined as a physical injury caused by external forces or violence. -Fifth leading cause of death in the United States. -Deaths related to trauma are primarily from motor vehicle crashes (MVCs), homicide, poisoning (e.g., prescription drug overdose), and falls. -Use of alcohol, drugs, or other substance abuse is often involved in traumatic events. -Trauma is frequently referred to as the disease of the young, because the majority of injured persons range in age from 16 to 54 years. -MVCs are the leading cause of death in teens; approximately 11 teens die in an MVC every day on U.S. roads. -Programs such as Graduated Drivers Licensing (GDL) are aimed at reducing teen MVC-related deaths through better driver safety education. -The incidence of trauma in the United States is a major health care and economic concern because of the loss of life, the societal burden in terms of lost productivity and increased disability of injured persons, and the consumption of health care resources. -A model trauma system provides an organized approach to trauma care that includes components of prevention, rapid access, acute hospital care, rehabilitation, and research activities. -Regional and state trauma systems provide comprehensive processes to deliver optimal care through an established trauma system network that matches a patient's medical needs to the level of trauma hospital with the resources necessary to provide the best possible care for the type and severity of traumatic injury. -A trauma system combines levels of designated trauma centers that coexist with other acute-care facilities. -Levels of a trauma system are a differentiation of medical care but are defined by resources available within the specific hospital. Levels of Trauma: -Level I: •Provides comprehensive trauma care •Regional resource center that provides leadership in education, research, and systems planning •Providers immediately available, including trauma surgeon, anesthesiologist, physician specialists, and nurses -Level II: •Provides comprehensive trauma care as a supplement to a Level I center, transfer to Level 1 if needed •Meets the same provider expectations for care as a Level I center •Is not required to participate in education and research -Level III: •Provides prompt, immediate emergency care and stabilization of patient with transfer to a higher level of care •Serves a community that does not have immediate access to a Level I or II center -Level IV: •Provides advanced trauma life support prior to transfer •Primary goal is to resuscitate and stabilize the patient and arrange for immediate transfer to a higher level of care -Mayo, Banner University, Honor Osborn and Honor Scottsdale, and St Joseph's are examples of Level 1 trauma centers -They treat the sickest of the sick -Level III trauma centers often can't do surgeries -Level IV trauma center is like an urgent care clinic Prevention: -Primary prevention: prevent the event •Driving safety classes •Speed limits •Campaigns to not drink and drive -Secondary prevention: minimize the impact of the traumatic event •Seat belt use •Airbags •Car seats •Helmets -Tertiary prevention: maximize patient outcomes after a traumatic event through emergency response systems, medical care, and rehabilitation Trauma Team: -Similar to code team -Team members preassigned -Emergency medical services (EMS) response team -Trauma surgeon (team leader) -Emergency physician -Anesthesiologist -Trauma nurse team leader (coordinates and directs nursing care) -Trauma resuscitation nurse (hangs fluids, blood, and medications; assists physicians) -Trauma scribe (records all interventions on the trauma flow sheet) -Laboratory phlebotomist -Radiologic technologist -Respiratory therapist -Social worker/pastoral services -Hospital security officer -Physician specialists (neurosurgeon, orthopedic surgeon, urological surgeon) -Sometimes have to divert trauma to another hospital if one hospital does not have enough room for the patient transfer - often called a code purple -A lot of trauma people come in and aren't able to give you information: social worker can help find their family members and contact them Trauma Triage: -Triage means sorting the patients to determine which patients need specialized care for actual or potential injuries. -Essential for determining if a patient needs to be transferred to a Level 1 trauma center -Triage decisions are often made by prehospital personnel based on knowledge of the mechanisms of injury and rapid assessment of the patient's clinical status. -The ultimate goal of any EMS system is to get the patient to the right level of hospital care in the shortest span of time to optimize patients' outcomes. -Additional lifesaving prehospital interventions that may be required include spinal precautions, occlusive dressings on open chest wounds, airway management and ventilation assistance, and needle thoracotomy to relieve tension pneumothorax. -Ground or air transport is appropriate to move the trauma patient from the scene of the injury to the trauma center. -Considerations in the choice of transport include travel time, terrain, availability of air and ground units, capabilities of transport personnel, and weather conditions. -Have to decide if patients are stable enough to be transferred in an ambulance or by air Primary Trauma Survey: -Identify life threatening conditions (what will kill them first), appropriate interventions started -The primary survey focuses on: •Airway/cervical spine •Breathing •Circulation •Disability (LOC, Glasgow Coma Scale) •Exposure (clothes off) •Facilitation of adjuncts and family (vital signs, family to stay) •Get resuscitation adjuncts -If uncontrolled external hemorrhage is noted, the usual ABC assessment format may be reprioritized to <C>ABC for hemorrhage control. -The <C> stands for catastrophic hemorrhage and, if present, needs to be controlled first. -Apply direct pressure with a sterile dressing followed by a pressure dressing to any obvious bleeding sites. -The primary survey aims to identify life-threatening conditions so that appropriate interventions can be started. -You may identify life-threatening conditions related to ABCs at any point during the primary survey. -When this occurs, start interventions immediately, before moving to the next step of the survey. -The alertness level of the patient can be an important factor for selecting appropriate airway interventions. -Determine level of consciousness (LOC) by assessing the patient's response to verbal and/or painful stimuli. -A simple mnemonic to remember is AVPU: •A = alert •V = responsive to voice •P = responsive to pain •U = unresponsive. Secondary Trauma Survey: -Begins addressing each step of primary survey -Start life saving interventions -Brief, systemic process to identify all injuries -Starts with history and head to toe assessment -Ends with log rolling patient to check back Traumatic Injuries: -Heat Related : heat cramps, heat exhaustion, heat stroke -Cold: frostbite, hypothermia, submersion -Bites: bug, animal and human -Stings: bee, scorpion -Poisonings: accidental or intentional -Violence -Terrorism -Mass Casualty

five level emergency severity index (ESI)

-ESI Level 1: patient requires immediate life-saving intervention -ESI Level 2: patient is in a high risk situation, is disoriented, in severe pain, or vitals are in danger zone -ESI Level 3: if multiple resources are required to stabilize the patient, but vitals are not in the danger zone -ESI Level 4: if one resource is required to stabilize the patient -ESI Level 5: if the patient does not require any resources to be stabilized

external fixation

-An external fixator is a metallic device composed of metal pins that are inserted into the bone and attached to external rods to stabilize the fracture while it heals. -The external fixator is attached directly to the bones by percutaneous transfixing pins or wires. -It can be used to apply traction or to compress fracture fragments and immobilize reduced fragments when the use of a cast or other traction is not appropriate. -The external device holds fracture fragments in place similar to a surgically implanted internal device. -External fixation is often used in an attempt to salvage extremities that otherwise might require amputation. -Because the use of an external device is a long-term process, ongoing assessment for pin loosening and infection is critical. -Infection (indicated by exudate, erythema, tenderness, and pain) may require removal of the device. -Pus oozing out of the hole, redness, swelling, elevated temperature, and elevated WBC indicates infection -Instruct the patient and caregiver about meticulous pin care. -Although each physician has a protocol for pin care cleaning, chlorhexidine 2mg/ml is often used. -Water and peroxide is used for pin site care

environmental emergencies

-Increased interest in outdoor activities such as running, hiking, cycling, skiing, and swimming has increased the number of environmental emergencies seen in the ED. -Illness or injury may be caused by the activity, exposure to weather, or attack from various animals or humans.

heat cramps

-Heat cramps are severe cramps in large muscle groups fatigued by heavy work. -Cramps are brief and intense and tend to occur during rest after exercise or heavy labor. -Nausea, tachycardia, pallor, weakness, and profuse diaphoresis are often present. -The condition is seen most often in healthy, acclimated athletes with inadequate fluid intake. -Cramps resolve rapidly with rest and oral or parenteral replacement of sodium and water -Elevation, gentle massage, and analgesia minimize pain -Patient should avoid strenuous activity for at least 12 hours -Emphasize salt replacement in future

abdominal trauma

-3rd leading cause of traumatic death after head and chest injuries -Blunt injuries more deadly than penetrating -25% require surgical intervention -Motor vehicle crashes most common type of blunt injury -Stab wounds and gunshots are most common penetrating injuries -Largest hollow space in the body, separated from the thoracic cavity by the diaphragm -Contains digestive tract, stomach, liver, pancreas, spleen, kidneys and adrenal glands, bladder -Entire cavity is lined with peritoneum

neurogenic shock

-Central nervous system dysfunction -Neurogenic shock, in contrast to spinal shock, results from loss of vasomotor tone due to injury and is characterized by hypotension and bradycardia. -Loss of sympathetic nervous system innervation causes peripheral vasodilation, venous pooling, and a decreased cardiac output. -These effects are generally associated with a cervical or high thoracic injury (T6 or higher).

fractures

-A fracture is a disruption or break in the continuity of the structure of bone. -Although traumatic injuries account for the majority of fractures, some fractures are secondary to a disease process (such as pathologic fractures from cancer or osteoporosis). Complications of Fracture Healing: -Delayed union: •Fracture healing progresses more slowly than expected. •Healing eventually occurs. -Nonunion: •Fracture fails to heal despite treatment. •No x-ray evidence of callus formation. -Malunion: •Fracture heals in expected time but in unsatisfactory position, possibly resulting in deformity or dysfunction. -Angulation: •Fracture heals in abnormal position in relation to midline of structure (type of malunion). -Pseudoarthrosis: •Type of nonunion occurring at fracture site in which a false joint is formed with abnormal movement at site. -Refracture: •New fracture occurs at original fracture site. -Myositis ossificans: •Deposition of calcium in muscle tissue at site of significant blunt muscle trauma or repeated muscle injury. Clinical Manifestations: -The clinical manifestations of fracture include immediate localized pain, decreased function, and inability to bear weight on or use the affected part. -The patient guards and protects the extremity against movement. -Obvious bone deformity may not be present. -If a fracture is suspected, the extremity is immobilized in the position in which it is found. -Unnecessary movement increases soft tissue damage and may convert a closed fracture to an open fracture or create further injury to adjacent nerves and blood vessels. Interprofessional Care: -The overall goals of fracture treatment are: (1) Anatomic realignment of bone fragments through reduction (2) Immobilization to maintain realignment, and (3) Restoration of normal or near-normal function of the injured part. Closed Fracture Reduction: -Closed reduction is a nonsurgical, manual realignment of bone fragments to their previous anatomic position. -Traction and countertraction are manually applied to the bone fragments to restore position, length, and alignment. -Closed reduction is usually performed while the patient is under local or general anesthesia (conscious sedation). -Immobilization afterwards: traction, casting, external fixation, splints, or orthoses (braces) Open Fracture Reduction: -Open reduction is the correction of bone alignment through a surgical incision. -It usually includes internal fixation of the fracture with the use of wires, screws, pins, plates, intramedullary rods, or nails. -The main risks of this form of fracture management are infection, complications associated with anesthesia, and the effect of preexisting medical conditions (e.g., diabetes). -Early ROM of joint to prevent adhesions -Open reduction facilitates early ambulation that decreases the risk of complications related to prolonged immobility. Drug Therapy: -Patients with fractures experience varying degrees of pain associated with muscle spasms. -Central and peripheral muscle relaxants, such as carisoprodol (Soma), cyclobenzaprine (Flexeril), or methocarbamol (Robaxin), may be prescribed for management of pain associated with muscle spasms. -The threat of tetanus from an open fracture can be reduced by administering tetanus and diphtheria toxoid or tetanus immunoglobulin for the patient who has not been previously immunized or whose immunization is expired. -Bone-penetrating antibiotics, such as a cephalosporin (e.g., cefazolin [Kefzol, Ancef]), are used prophylactically before surgery. -These drugs make you sleepy: teach patients not to drive when they are on them -Amputees will always be given tetanus shots Obtain the following health information from the client: -Past health history: traumatic injury; long-term repetitive forces (stress fracture); bone or systemic diseases, prolonged immobility, osteopenia, osteoporosis -Medications: use of corticosteroids (osteoporotic fractures); analgesics -Surgery or other treatments: first aid treatment of fracture, previous musculoskeletal surgeries -Also obtain the following important health information related to pertinent functional health patterns: -Health perception-health management: estrogen replacement therapy, calcium supplementation -Activity-exercise: loss of motion or weakness of affected part; muscle spasms -Cognitive-perceptual: sudden and severe pain in affected area; numbness, tingling, loss of sensation distal to injury; chronic pain that increases with activity (stress fracture) Immediate Emergency Management: -Mechanism of Injury: •Blunt trauma •Penetrating trauma •Seizure •Crush injury -Overall stability needs to be determined: •ABCs/CABs •LOC, VS •Control bleeding •IV access, fluids, blood products Acute Care: -Patients with fractures can be treated in the emergency department or a physician's office -Patients are released home, or they may require hospitalization -Severe life threatening orthopedic injuries require immediate care and are at risk for systemic volume blood loss or loss of limb function -Specific nursing measures depend on the setting and type of treatment.

poisonings

-A poison is any chemical that harms the body accidentally, occupationally, recreationally, or intentionally. -More than 5 million cases of human poisonings occur each year in the United States. -Natural or manufactured toxins can be ingested, inhaled, injected, splashed in the eye, or absorbed through the skin. -Severity of the poisoning depends on type, concentration, and route of exposure. -Toxins can affect every tissue of the body, so symptoms can be seen in any body system. -Tylenol overdoses: seen most often in teenage girls -Cyanide seen from smoke inhalation from burning materials Treatment: -Don't mix Comet cleaner and Clorox bleach together -Specific management of toxins involves decreasing absorption, enhancing elimination, and implementing toxin-specific interventions. -If poison or drug is injected into veins, use hemodialysis to help get it out -Can also use activated charcoal, dermal cleansing, eye irrigation, and gastric lavage -Consult the local poison control center 24 hours a day for the most current treatment protocols for specific poisons. -Gastric lavage involves oral insertion of a large-diameter (36F to 42F) gastric tube for irrigation of copious amounts of saline. -Patients with an altered LOC or diminished gag reflex are intubated before lavage. -To be effective, perform gastric lavage within 1 hour of ingestion of most poisons. -Patients who ingest caustic agents, co-ingest sharp objects, or ingest nontoxic substances should not receive lavage. -Problems associated with lavage include esophageal perforation and aspiration. -The most common and effective intervention for management of poisonings is administration of activated charcoal orally or via a gastric tube within 1 hour of poison ingestion. -Many toxins adhere to charcoal and pass through the gastrointestinal (GI) tract rather than being absorbed into the circulation. -Activated charcoal does not absorb ethanol, hydrocarbons, alkali, iron, boric acid, lithium, methanol, or cyanide. -Adults receive 50 to 100 g of charcoal. For some toxins (e.g., phenobarbital, digoxin) multiple-dose charcoal may be required. -Contraindications to charcoal administration include diminished bowel sounds, paralytic ileus, and ingestion of a substance poorly absorbed by charcoal. -Skin and ocular decontamination involves removal of toxins from skin and eyes using copious amounts of water or saline. -"The solution to pollution is dilution" -Most toxins, with the exception of mustard gas, can be safely removed with water or saline. -Water mixes with mustard gas and releases chlorine gas. -Lavage off liquids -As a rule, brush dry substances from the skin and clothing before using water. -Do not remove powdered lime with water. -It should just be brushed off. -Wear personal protective equipment (PPE) (e.g., gloves, gowns, goggles, respirators) for decontamination to prevent secondary exposure. -Decontamination procedures are usually done by those specially trained in hazardous material decontamination before the patient arrives at the hospital and again at the hospital, if necessary. -Decontamination takes priority over all interventions except those needed for basic life support.

low blood flow hypovolemic shock

-Absolute hypovolemia: loss of intravascular fluid volume: •Hemorrhage: injury or trauma •GI loss (e.g., vomiting, diarrhea) •Fistula drainage •Diabetes insipidus •Hyperglycemia •Diuresis -Response to acute volume loss depends on extent of injury, age, and general state of health -An overall assessment of physiologic reserves may indicate the patient's ability to compensate. -A patient may compensate for a loss of up to 15% of the total blood volume (approximately 750 mL). -Further loss of volume (15% to 30%) will result in a sympathetic nervous system (SNS)-mediated response. -This response results in anxiety, tachypnea, an increase in heart rate, CO, and respiratory rate and depth. -Stroke volume, urinary output, central venous pressure (CVP), and PAWP are decreased because of the decreased circulating blood volume. -If volume loss is greater than 30%, compensatory mechanisms may fail and immediate replacement with blood products should be started. -Loss of autoregulation in the microcirculation and irreversible tissue destruction occur with loss of more than 40% of total blood volume. -Common laboratory studies and assessments that are done include serial measurements of hemoglobin and hematocrit levels, electrolytes, lactate, blood gases, central venous oxygenation (SvO2), and hourly urine outputs. Interprofessional Care: -Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = volume expansion -One or two large-bore IV catheters (14 to 16 gauge), intraosseous access device, or central venous catheter -Isotonic crystalloids (e.g., normal saline, lactated Ringers) and colloids (e.g., albumin) have a role in fluid resuscitation -Fluid responsiveness is determined by clinical assessment: •Vital signs •Cerebral and abdominal pressures •Capillary refill •Skin temperature •Urine output: foley with urometer •Hemodynamic parameters, such as SVV or CO, are also used. •Monitor trends in BP with an automatic BP cuff or an arterial catheter to assess the patient's response. -Two major complications of large volumes (hemodilution changes blood osmolarity): •Hypothermia •Coagulopathy -Persistent hypotension after adequate fluids-must fill the tank first •Vasopressor (e.g., norepinephrine [Levophed], dopamine [Intropin]) and/or an inotrope (e.g., dobutamine [Dobutrex]) may be added for vasoconstriction effect -The goal for fluid resuscitation is restoration of tissue perfusion

cerebral edema

-Cerebral edema is defined as an increased accumulation of fluid in the extravascular spaces of brain tissue. -There are a variety of causes, including mass lesions, head injuries, cerebral infection, vascular insult, and toxic or metabolic encephalopathy. -Other causes include a brain tumor, abscess, toxins, fluid shifts (extracellular/ intracellular, SIADH, glucose shifting due to HHS and DKA), cerebral spinal fluid, and hydrocephalus -Regardless of the cause, cerebral edema results in an increase in tissue volume that can increase ICP. -The extent and severity of the original insult are factors that determine the degree of cerebral edema. -There are three types of cerebral edema: vasogenic, cytotoxic, and interstitial. More than one type may occur in the same patient.

tetanus immunizations

-Include in medical history when last immunization was -Tetanus immunizations are good for 10 years unless they sustain a wound, then it is given if it is more than 5 years -Given in any injury if anaerobic metabolism of organisms may occur -Types of immunizations or passive/immediate immunity TIG (immune globulin): •Td: Tetanus-diphtheria toxoid •Tdap: Tetanus, diphtheria, acellular pertussis •TIG: Tetanus immune globulin (human) -Unimmunized (unknown): should give booster AND TIG for high risk wounds -Immunized but GREATER than 5 years: high risk wound, should give booster -The Provider will determine client need based on wound -Anytime the skin is open, the patient is at risk for tetanus -Need to know when the patient's last tetanus shot was -If patient is unresponsive, just give tetanus shot anyway: unless they are allergic to vaccine -Goal is to prevent patient from getting lockjaw

internal fixation

-Internal fixation devices (pins, plates, intramedullary rods, and metal and bioabsorbable screws) are surgically inserted to realign and maintain position of bony fragments. -These metal devices are biologically inert and made from stainless steel, vitallium, or titanium. -Proper alignment and bone healing are evaluated regularly by x-rays.

cauda equina syndrome

-Result from damage to cauda equine (lumbar and sacral nerve roots) -Asymmetrical distal weakness, patchy sensation in lower extremities. -May cause flaccid paralysis of lower extremities. -Complete loss of sensation between legs and over buttocks, inner thighs, and backs of legs (saddle area). -Areflexic (flaccid) bladder and bowel. -Severe, radicular, asymmetric pain. -Call the doctor if this occurs!

vertebral immobilization

-The body jacket brace is used for immobilization and support for stable spine injuries of the thoracic or lumbar spine. -The brace goes around the chest and abdomen, extending from above the nipple line to the pubis. -After application of the brace, assess the patient for the development of superior mesenteric artery syndrome (cast syndrome). •This condition occurs if the brace is applied too tightly, which results in compression of the superior mesenteric artery against the duodenum. •The patient generally complains of abdominal pain, abdominal pressure, nausea, and vomiting. •Assess the abdomen for decreased bowel sounds (a window in the brace may be left over the umbilicus). •Treatment includes gastric decompression with a nasogastric (NG) tube and suction. -Assessment also includes monitoring respiratory status, bowel and bladder function, and areas of pressure over the bony prominences, especially the iliac crest. -The brace may need to be adjusted or removed if any complications occur.

animal bites

-Animal bites from dogs and cats are most common, with wild or domestic rodents (e.g., squirrels, hamsters) following as the third most frequently reported offenders. -Dog bites usually occur on the extremities. -However, facial bites are common in small children. -Most victims own the dogs that bite them. -Dog bites may involve significant tissue damage with deaths reported, usually in children. -A plastic surgeon should evaluate all disfiguring wounds of the face. -Human bites also cause puncture wounds or lacerations. -These carry a high risk of infection from oral bacterial flora, most commonly Staphylococcus aureus, Streptococcus organisms, and hepatitis virus. -Infection rates are as high as 50% when victims do not seek medical care within 24 hours of injury. -Very important to irrigate animal bites, especially when they are on the face Treatment: -Wound care: irrigation and debridement -Suture: primary closure in facial wounds (rarely infected because well vascularized) -Delayed closure: heavily contaminated (dirty), significant amount of tissue damage, hands or lower extremities, or wound older than 6 hours -Some wounds are never sutured -Consider rabies postexposure prophylaxis in the management of all animal bites. -Transmission: •Saliva from the bite of an infected animal •Scratches and by contact with infected secretions through mucous membranes. -Any warm-blooded mammal (e.g., dogs, raccoons, bats) can carry rabies: •If an animal attack was not provoked •Involves a wild animal •Domestic animal not immunized against rabies •REQUIRED rabies postexposure prophylaxis when the animal is not found or a wild animal causes the bite -Hanging skin will get cut off -Wounds usually left open -Consider rabies postexposure prophylaxis in the management of all animal bites. -Rabies is generally transmitted via saliva from the bite of an infected animal. -It can also be spread by scratches and by contact with infected secretions through mucous membranes. -Any warm-blooded mammal (e.g., dogs, raccoons, bats) can carry rabies. -Consider rabies exposure if an animal attack was not provoked, involves a wild animal, or involves a domestic animal not immunized against rabies. -Always provide rabies postexposure prophylaxis when the animal is not found or a wild animal causes the bite.

cerebral blood flow

-Cerebral blood flow (CBF) is the amount of blood in milliliters passing through 100 g of brain tissue in 1 minute. -The global CBF is approximately 50 mL/min per 100 g of brain tissue. -The maintenance of blood flow to the brain is critical because the brain requires a constant supply of oxygen and glucose. -The brain has the ability to regulate its own blood flow in response to its metabolic needs despite wide fluctuations in systemic arterial pressure. -Autoregulation is the automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow during changes in arterial blood pressure (BP). -The purpose of autoregulation is to ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits. -The lower limit of systemic arterial pressure at which autoregulation is effective in a normotensive person is a mean arterial pressure (MAP) of 70 mm Hg. -Below this, CBF decreases, and symptoms of cerebral ischemia, such as syncope and blurred vision, occur. -The upper limit of systemic arterial pressure at which autoregulation is effective is a MAP of 150 mm Hg. -When this pressure is exceeded, the vessels are maximally constricted, and further vasoconstrictor response is lost. -The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. -CPP is equal to the MAP minus the ICP (CPP = MAP - ICP). -Normal CPP is 60 to 100 mm Hg. -As the CPP decreases, autoregulation fails, and CBF decreases. -A CPP less than 50 mm Hg is associated with ischemia and neuronal death. -A CPP less than 30 mm Hg results in ischemia and is incompatible with life. -Normally, autoregulation maintains an adequate CBF and perfusion pressure primarily by adjusting the diameter of cerebral blood vessels and metabolic factors that affect ICP. It is critical to maintain MAP when ICP is elevated. -This formula is clinically useful, although it does not consider the effect of cerebral vascular resistance. -Cerebral vascular resistance, generated by the arterioles within the cranium, links CPP and blood flow as follows: CPP = Flow x Resistance. -When cerebral vascular resistance is high, blood flow to brain tissue is impaired. -Transcranial Doppler is a noninvasive technique used in ICUs to monitor changes in cerebrovascular resistance. -CO2 constricts cerebral blood vessels -O2 hypoxia causes dilation of cerebral blood vessels -Lactic acidosis causes more dilation -Hydrogen ion concentration: acidosis, alkalosis -Breakdown in body ability to regulate -Herniation: if fluid runs out too fast, the brain tissue will move to another place -Lactic acidosis greater than 4 is a danger zone