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Identify the asessment criteria and resuscitative interventions for airway and C-spine control during the primary survey of the trauma patient.
- Airway obstruction: clear airway, suction if necessary, oral endotracheal tube if needed. Use of paralytic (succinylcholine).
- C-spine injury: always assume present, immobilize, do not hyper extend (use jaw thrust method), hard collar, HOB <30
Identify the assessment criteria and resuscitative interventions to support breathing during the primary survey.
Assess for spontaneous respirations, rate, and effort, patterns, asymmetrical chest movements, cyanosis, distended neck veins, tracheal shift. High flow 100% O2, 12L/min nasal cannula, mask or vent. Obatian O2 sats and ABGs. CT or chest x-ray
Life threatening thoracic injuries
- Ruib fractures: most common
- Inhalation injuries: soot around lips, singed nasal hair; get to burn center
- Tension Pneumo: needle decompression (14g, 2nd ICS)
- Open Pneumo: cover with vasaline gauze
- Massive Hemothorax: chest tube (cavity can hold 40% total blood volume)
- Flail Chest: mechanical positive pressure ventilation acts as splint
- Cardiac Tamponade: pericardial needle, surgery
- Injuries to great vessels: i.e. aorta
Identify the assessment criteria and resuscitative interventions to support circulation during the primary survey.
- Assume shock on any patient who is cool and pale with HR >120.
- Cardiac monitor (dysrhythmias)
- Pulse is a good estmate of CO
- Peripheral pulses may be absent
- Capillary blanche is a good estimate of volume status (delayed refill >2-3 sec hypovolemic)
- Maintain systolic >90
- Direct pressure to control bleeding
- Treat as shock until proven otherwise
What are the principles of fluid resuscitation based on the ACD classification of Hemorrhage?
- Establish vascular access and begin infusion if not already in place-2 peripheral IV lines with large bore (14-16 B) catheters and /or a central line /or intraosseous access
- "Rapid Infuser" fluid challenge to assess presence of hypovolemia
- Use trauma tubing to rapidly infuse large volumes
What are the characteristics/availability of each type of blood used for resuscitation of a trauma patient?
- Draw blood for ABG’s, H&H, Type & Cross match- may infuse blood now or later
- O Negative-universal donor, readily available
- Type specific (not cross matched), received within ½ hour
- Fully cross matched-received within 1 hour
- A: Allergies
- M: Medication
- P: Past illness/pregnancy
- L: Last meal
- E: Events (mechanism of injury)
- H: Head-to-toe assessment, use log roll tech to assess posterior
What is the significance of knowing the mechanism of injury in assessing and treating a trauma patient?
Helps identify injuries that aren't immediately evident and gives additional criteria
The medication used to improve blood flow and decrease edema in the initial phase of treatment for spinal cord injury (SCI) is?
- Methylprednisolone (Depomedrolor Solumedrol) Protocol
- IV bolus within 8 hours post SCI then continuous infusion for 23 hours
- Intent is to improve blood flow and decreases edema of spinal cord
- Lack of clear undisputable evidence to support practice and potential side effects are considerations in choice to administer.
List the options for immobilization of the cervical spine during the acute phase of injury
- Cervical skeletal traction: to immobilize and reduce the fracture or dislocation
- Skull tongs: attached to ropes, pulleys and weights. skin assessment over pessure areas and pin care, kinetic bed for constant turning to prevent pressure ulcers and pulmonary problems
- Halo Device: for stable injures and post tong removal (usually 2-4 weeks)
- Surgical stabilization/decompression: surgery based on criteria indicating surgery would improve recovery
- Hourly neuro assessments initially: same as with head injury
List the options for immobilization of thoracic and lumbar spine injuries
- Surgical stabilization: decompression laminectomy with or without fusion of spinal segments and insertion of stabilizing rods.
- Braces: most often used with thoracic and lumbar injuries ("turtle vest")
What are the clinical maifestations of spinal shock and how do these change as spinal shock resolves?
- Menifestations: flaccid paralysis, absence of deep tendon reflexes, absence of cutaneous sensation and urinary and fecal retention
- Resolution: return of reflexes, development of hyperreflexia rather than flaccidity, and return of reflex emptying of the bladder indicate that spinal shock is resolving
What are the interventions associated with each of the clinical problems that occur due to loss of sympathetic vasomotor tone?
- Lesions of the cervical and thoracic spine disrupt the descending sympathetic pathways thereby leading to peripheral vasodilation and hypotension.
- If the lesion is at T6 or above, sympathetic tone to the heart is compromised leading to unopposed vagal response and bradycardia, producing the neurogenic shock triadof bradycardia, hypotension, and peripheral vasodilation.
What are the measures used to prevent and/or treat Neurogenic Shock?
- Hemodynamic goal- systolic BP > 90mmHg, MAP 85-90mmHg for 7 days post injury to ensure perfusion of cord
- Volume expanders
- Hemodynamic monitoring to assess
- Prevention of postural hypotension-seen in cervical injuries especially
- Change positions slowly
- Tilt table with early mobilization
- Belly binder to prevent pooling of venous blood
What are the measures used to prevent and/or treat DVT and pulmonary emboli?
- Usual S&S may not be present so need to measure leg and thigh girth for swelling, malaise, and low grade temp of unknown origin
- Low molecular weight heparin or heparin
- Anti-embolic hose or pneumatic compression
- Insert inferior vena cava filter if prolonged
What are the measures used to prevent and/or treat loss of thermoregulation (poikilothermia)?
- Body temperature varies with environmental temperature due to loss of SNS communication with hypothalamus
- No peripheral input to brain
- No vasoconstriction, perspiration or piloerection below injury
- Maintain constant environmental temperature
What are the measures used to prevent and/or treat GI and bowel problems?
- Constipation, paralytic ileusand abdominal distention (can increase respiratory distress) due to loss of autonomic tone and bowel atony during spinal shock
- Use NG tube for decompression until bowel sounds return usually within 72 hours-assess for return of bowel sounds
- Use H2 receptor blockers famotidine(Pepcid) and/ or proton pump inhibitors pantoprazole(Protonix)
What are the measures used to prevent and/or treat bladder problems?
- atonyduring spinal shock leads to retention of urine
- Insert Foley-strict aseptic technique, maintain patency
- Strict I&O
- Ensure adequate fluid intake to prevents UTI and renal calculi
- Monitor BUN and creatinine levels
- UTI-suspect if fever/chill of unknown origin, elevated WBC
- Urine cultures if signs of infection
- Remove Foley once spinal shock resolves and institute bladder management program as ordered
What are the foci of care during the sub acute phase of care of the SCI patient?
- Psychological assessment -fear of death, loss and grieving, family life style/routines totally disrupted
- Assess family and individual coping mechanisms
- Create a trusting safe environment
- Support decision making process of both patient and family
- Assess learning needs
- Assessment of vitals, neuro, respiratory status q 8 hours
- Integumentary assessment (at risk for skin breakdown due to impaired circulation, lack of sensation and immobility)
- Atrophy of muscles tends to occur during flaccid stage and contractures during spastic state
- Fluid and nutrition management
- Neurogenic bowel management depends on level & syndrome of injury
- Spastic bowel with CSI’s-reflexive incontinent until trained
- Flaccid (limp) bowel with lumbar or sacral injuries-Constipated with flaccid paralysis.
- Neurogenic bladder management depends on level & syndrome of injury
- Spastic bladder with CSI’s-reflexive incontinence.
- Flaccid bladder results in partial emptying and continual dribbling of small amounts of urine
- Sensory deprivation-loss of sensation below the level of injury
- Remember that cognitive ability is not affected
- Stimulate- they can still see, hear, talk, smell, taste
- May have sleep disturbances and vivid dreams initially
What are the most common symptoms associates with autonomic dysreflexia?
- Pounding headache
- Hypertension (blood pressure greater than 200/100)
- Nasal Congestion
- Flushed (reddened) face, goose pimples, sweating, red blotches on the skin above injury abovethe level of injury
- Cold, clammy skin belowlevel of spinal injury
What are the priority interventions for suspected autonomic dysreflexia?
- Place in upright position and loosen any restrictive clothing
- Monitor BP-will be elevated above baseline
- Check the urinary drainage system first and correct the problem if present
- Is the drainage bag full?
- Is there a kink in the tubing?
- Is the drainage bag at a higher level than the bladder?
- Is the catheter plugged?
- Catheter may need to be changed if not draining in 2-3 minutes
- Suspected cause = bowel?
- Impaction? digital evacuation / enema
- Use anesthetic ointment
What are the medications used for autonomic dysreflexia?
- Used only if the offending trigger/stimulus cannot be identified and removed -or when an episode persists even after removal of the suspected cause.
- Nifedipine(Procardia)-10 mg. p.o./sublingual
- Nitroglycerine-1/150 sublingual or 1/2 inch Nitropaste topically
- Clonidine(Catapres)-0.1 to 0.2 mg. p.o. Hydralazine(Apresoline) -10 to 20 mg. IM/IV
- Chronic (recurrent episode prevention)
- Prazosin (Minipress) -0.5 to 1.0 mg. daily
- Clonidine (Catapres) -0.2 mg. p.o. twice daily
What are the most likely causes of autonomic dysreflexia?
- Bladder (most common)-from overstretch or irritation of bladder wall
- Urinary tract infection
- Urinary retention
- Blocked catheter
- Overfilled collection bag
- Non-compliance with intermittent catheterization program
- Bowel-over distention or irritation
- Constipation / impaction
- Distention during bowel program (digital stimulation)
- Hemorrhoids or anal fissures
- Infection or irritation
What are the less common causes of autonomic dysreflexia?
- Skin-related disorders
- Any direct irritant below the level of injury (eg. -prolonged pressure by object in shoe or chair, cut, bruise, abrasion)
- Pressure sores (decubitus ulcer)
- Ingrown toenails
- Burns (e.g. -sunburn, burns from using hot water)
- Tight or restrictive clothing or pressure to skin from sitting on wrinkled clothing
- Sexual activity
- Menstrual cramps
- Labor and delivery
What are the characteristics of subdural hematomas?
- Bleeding from veins (usually) or arteries into the subdural space between the dura and the covering of the brain.
- If venous bleed, hematoma develops slowly
- Acute(within 24-48hours), subacute(within 48hr-2 weeks) or chronic(weeks to months post injury due to repeated small bleeds)
- Frequently associated with skull fractures
- Carries the highest mortality and poorest prognosis of hematomas
- Clinical manifestations are related to increased intracranial pressure (ICP).
- If GCS <9 should have intracranial pressure monitoring
- Surgical evacuation if large
What are the characteristics of epidural hematomas?
- Arterial bleeding between the dura and the skull
- Life threatening emergency –rapid surgical intervention
- S&S occur rapidly consciousness followed by a lucid period then decreased LOC, head ache, N&V and focal neurologic deficits15-20% mortality even with immediate surgical evacuation
- Often seen in children and young adults
What are the systemic events that contribute to secondary traumatic brain injury (TBI) and increased ICP?
- Anything that increases metabolic demand or reduces blood/oxygen supply to the brain
- Hypotensive episodes
- Electrolyte imbalances
- Infection, fever andsystemic inflammatory response
- Increased intra-abdominal/
- thoracic pressure
Identify the interventions used during the preoperative/emergency management/resuscitative phase to treat severe TBI and prevent secondary injury
Avoidance of hypotension and hypoxia is key to prevention/minimization of secondary injury
- CT scan of head and cervical spine: for rapid diagnosis in those at high risk to determine extent of injury
- – GCS less than 13
- – open or depressed skull fracture
- – any sign of basilar skull fracture: panda eyes, CSF ear leak, Battles sign (direct entry to brain)
- – seizure
- – focal neurological deficit
- – vomiting more than x1
- – amnesia lasting longer than 30 minutes
Identify the interventions used during the operative management phase to treat severe TBI and prevent secondary injury
- Not everyone goes through this phase
- Maintain ICP < 20 mmHg (normal is <15mmHg)
- Maintain CPP > 60-70mmHg (normal is 50-150mmHg)
Identify the interventions used in the first tier of the critical care phase
- Avoid hypotension
- Use of Hypertonic saline (3%) as initial resuscitation fluid - maintain Na+ at upper limits
- Vasopressors if needed
- Avoid hypoxia (PaO2>60, Ht 30-33%)
- Avoid hypercarbia (maintain PaCO2 35-45) leads to vasodilation, increases ICP
- Avoid anything that increases metabolism (early anticonvulsant /dilantin therapy for high risk patients for 1st week)
- Nutritional feeding
- Preventing intracranial infection
- Aggressive glucose control
Identify the interventions used in the second tier of the critical care phase
- CT scan to re-evaluate
- CSF drainage to maintain ICP 20-25
- Diuretics - start with loop (lasix or edecrin)
- Increase Na+>145 with 3% saline
- Intermittent IV bolus of Mannitol (used for strong diuresis, can cause hypotension, rapid electrolyte changes)
- Increase sedation (propofol), decrease pain (fentanyl), decrease anxiety (versed or ativan)
- Temporary hyperventilation to reduce CO2
Identify the interventions used in the third tier of the critical care phase
- Barbituate coma (pentobarbital): last ditch effort
- Neuromuscular blocking agent: Norcuron
- Decompression hemicraniectomy: allows to swell, immediate drop in ICP (cause your head is cut open)
- Decompression laprotomy: reduce fluid in abdomen
- Moderate hypothermia: probably to lower metabolic demand (not really in the notes)
Glasgow Coma Scale
- Motor Response
- 6 -Obeys commands fully
- 5 -Localizes to noxious stimuli
- 4 -Withdraws from noxious stimuli
- 3 -Abnormal flexion, i.e. decorticate posturing
- 2 -Extensor response, i.e. decerebrate posturing
- 1 -No response
- Verbal Response
- 5 -Alert and Oriented
- 4 -Confused, yet coherent, speech
- 3 -Inappropriate words and jumbled phrases consisting of words
- 2 -Incomprehensible sounds
- 1 -No sounds
- U= untestable
- Eye Opening4 -Spontaneous eye opening
- 3 -Eyes open to speech
- 2 -Eyes open to pain
- 1 -No eye opening
Central stimulation techniques
- Used to test motor response, brain function
- Trapezius Squeeze
- Supraorbital Pressure
- Mandibular Pressure
- Sternal Rub
Peripheral stimulation techniques
- Used to test LOC, eye opening and verbal response
- Nail bed pressure with pencil over half moon as hard as you can
- Sinus bradycardia
- Systolic hypertension with widening pulse pressure
- Irregular respiratory pattern (Cheyne-Stokes)
Factors that contribute to transient increases in ICP
- HypercapniaPaCO2 <45mmHg/Hypoximia
- Cerebral dilating agents (anithistamines)
- Prone position, flexion of neck and hip-elevate HOB
- Isometric muscle contractions
- Coughing or sneezing
- Rapid eye movement sleep
- Arousal from sleep
- Emotional upset
- Clustering of care activities
Used to confirm presence to CSF in drainage from nose or ear
Causes of ischemic stroke
- Thromotic-large artery stroke due to atheroscleroticthrombus or hypoperfusion(>16%)
- • Valvularheart disease
- • Atrial fibrillation
- • MI/heart failure/aneurysm
- • Cardiomyopathy
- • Iatrogenic-IABP/CABG/PTCA
- Cryptogenic-unknown (>36%)
- Lacunar-smalldistal artery occlusion due to stenosis or embolic event (<16%)
- Other (>2%)
What is the most important point in the initial history of those with suspected ischemic stroce in relation to treatment?
Establish onset of symptoms (like when I cracked Danielle in the head for mouthing off)
What is the diagnostic study that is used to rule out stroke due to hemorrhage?
CT (we hope, that's all we could find, this packet is crap)
What is the treatment for those who present with ischemic stroke within 3-4.5 hours of the onset of symptoms (facial droop, arm drift, and abnormal speech)?
- Recombinant tPA (rtPA)
- Contraindications: bleeding risks, resolution of symptoms
- Wait 48 hours after administration to give antiplatelet meds (ASA/Plavix) or anticoagulants
What is the most important risk factor for hemorrhagic stroke as well as the most effective means of prevention?
Hypertension, get that shit under control!
What are the two most common causes of hemorrhagic stroke?
- Subarachnoid Hemmorhage (SAH): due to rupture of cerebral aneurysm, arterial venous malformation
- Intracerebral Hemmorhage (ICH): due to rupture of a vessel, cause more than twice the number of strokes as SAH, very poor prognosis
What are the most common causes and symptoms of SAH and its treatment?
- Causes: rupture of cerebral aneurysm, arterial venous malformation
- Symptoms: worst headache EVER, brief loss of consciousness, N/V, focal neuro deficits, stiff neck due to irritation of meninges
- Treatments: Triple H Therapy, Nimodipine (Nimotop), cerebral angioplasty
Triple H Therapy
- Improve blood flow and cardiac output
- Hypertension: maintain systolic 150 to ensure adequate pressure to push blood through spasm
- Hypervolemia: helps maintain pressure
- Hemodilution: decreases viscosity of blood
Identify the major components of collaborative management of stroke
- Differentiate the cause of the stroke
- Implement treatment according to cause of bleed
- Airway, Airway, Airway (get it yet?)
- Provide ventilatory assistance as required
- Perform frequent neuro assessments
- Maintain surveillance for complications
- Provide comfort and emotional support
- Design and implement appropriate rehab program
- Educate, Educate, Educate the hell out of them