Neurological Assessment and Management of Traumatic Brain Injury and Spinal Cord Injury, Exams of Nursing

Download Neurological Assessment and Management of Traumatic Brain Injury and Spinal Cord Injury and more Exams Nursing in PDF only on Docsity! [Date] Page 1 Critical Care Exam 3 Guide Assured Success 100% Neuron Basics · Brain metabolism o Soul source of energy for the brain is glucose. Brain needs glucose to function. Brain cannot store it, but needs a constant supply. If glucose levels start to fall you will some changed. o Cerebral glucose < 70 mg/ld. = confusion o Cerebral glucose < 20 mg/ld. = damage · Cerebral blood flow · Auto regulation o Changes in pressure o Changes in CO2 ▪ Alters cerebral blood volume with change in blood vessel size o Ability of the blood vessel in the brain to either constrict or dilate in response to pressure or CO2 levels ▪ Hypotension or hypo ventilating causing hypercapnia BV in brain will dilate and vice versa try to send more blood and oxygen to brain. ▪ If hypertension or hypomania blood vessels in the brain will constrict. ▪ Systolic less than 50 or greater than 160 BV in brain lose the ability to auto regulate. Neuron Assessment o GCS, LOC, Memory, speech, Reflexes (Babinski with brain injury) which only babies should have if adult has it this is not good, motor response, sensation , look for aphasia, motor strength ▪ Concerned with GAS or 8 or lower o Posturing ▪ Decorticate [Date] Page 2 · Extremities go toward the body ▪ DE cerebrate · Extremities pull away from the body, more severe, damage to brainstem – this is the worse posturing · Cranial nerves o 1 – Olfactory - Smell o 2 – Optic - vision, pupil response, visual fields – PERRLA - need flashlight or pen light dim the lights in room o 3, 4, 6 - Coulometer, Trochlear, Abduces - eye movement – 6 fields of gaze “EOM’S” [Date] Page 5 · Optimal is 70-100 mmHg · If less than 70 you can develop ischemia to brain tissue. · If under decrease BP or increase ICP ▪ If CPP is inadequate, ischemia or infarction can occur · Increased Intracranial Pressure o Associated with many neurological problems O ICP 20mm Hg or greater for 5 minutes or longer Increased metabolic de- minds, fevers, seizures can also increase in- tracranial pressure. o Results from an increase in any one of the three com- po- nents: ▪ Increased Blood Volume · Loss of Autoregulation · Decreased Oxygenation · Hypercapnia – cause blood vessels in brain to dilate sending more blood to brain which can increase pressure · Obstruction – Ex: Tumor ▪ Increased Brain Volume · Cerebral Edema ▪ Increased Cerebrospinal Fluid · Hydrocephalus o Cardinal (early) sign is changes in LOC o Pupil changes, respiratory changes are late sign o Herniation = he dead ▪ Brain usually comes out of foramen magnum ▪ Nurse needs to identify signs early. Prevention es may important. ▪ If ICP > 20 for 5 minutes or more herniation can occur. [Date] Page 6 ▪ We need to know the signs to look for to prevent herniation to occur. ICP Monitoring · Indications o Severe head injury, severe neurologic disorder, GCS < 8, Post brain surgery, tumors, strokes · Purpose [Date] Page 7 o Severity of brain impairment, diagnose problems, assess responsiveness to therapy, au- mint our assessment · Placement o Most placed in the ventricle because you can drain CSF also o Mostly placed in OR but can be placed at bedside o Only placed by neuron surgeon. · Transducer System o Fluid Filled o Microchip o Fiber optic Catheter o Monitors can be placed in different areas of the brain, but most monitors will be places in the ventricles, most of these monitors have the ability to drain CSF as well. · Nursing Management o During Placement ▪ Set up equipment ▪ Maintain asepsis ▪ Dress the site after its been placed ▪ Document o During ICP monitoring ▪ Hourly neuron checks, hourly vitals (MAP, ICP, CPP), maintain sterility, monitor form complications (hemorrhage, infection), biggest complication is infection. Huge risk is also meningitis. · Cerebral Oxygenation Monitoring o Jugular Oxygen Saturation ▪ Monitored via a fiber optic catheter ▪ Normal value 60%-70% · Does not ensure adequate perfusion ▪ Values < 50% indicate ischemia o Partial Pressure of Brain Tissue Oxygen 10[Date] Page 10 o Preoxygenate beforehand. o Limit suction to 10 seconds. No more then 2 to 3. · Assessment o Neurological exam hourly. o Vital signs 11[Date] Page 11 ▪ Cushing’s triad (bad) – never want to see this. ICP is so high that it is putting pressure on brainstem. · Hypertension, Bradycardia, Abnormal respiratory rate and pattern · Last thing before the patient herniates · If patient has this. Sit the patient up as high as possible (high fowlers). Patient will need surgery there is not much the nurse can do. · Nursing activities o Avoid clustering of activities o Avoid valsalva situations ▪ Pooping, coughing, and vomiting. Can give stool softeners for poop. Vomiting can put in NG or give them an antiemetic. o Minimize external stimuli ▪ Noise, light, activities. No more then 2 family members in room. Keep it quiet. ICP Medical Management · Adequate Oxygenation o Goal: PaO2 > 80mm Hg o Maintain O2 and CO2 levels. o Airway vigilance o Mechanical ventilation o Use PEEP with caution – decreases venous returns. If not in heart could be in brain because it’s everywhere. Typically won’t see more then 5 of peep. o Adequate hematocrit · Carbon Dioxide Management o PaCO2 35-45 mm Hg o Avoid hyperventilation unless you see Cushing Triad. · Diuretics o Osmotic and Loop diuretics ▪ Reduce brain tissue volume (cerebral edema) · Manito – drug of choice, crosses BBB – pulls the sodium and 12[Date] Page 12 water out of the brain tissue so you can pee it out) · Hypertonic saline (use caution and patient must have a central line) 2nd choice and keep a close eye on sodium level. · Steroids o Dexamethasone – also known as dead-on preferred 15[Date] Page 15 ▪ Remove part of the skull to allow brain to swell ▪ Bone flap placed in the abdomen ▪ Patient will need to wear helmet · Psychosocial Support o Patient , Family, Support, Information, Chaplain or social services Traumatic Brain Injury · Skull Fractures o Open vs. Closed ▪ Cranium open and brain exposed or closed o Linear skull fracture ▪ Basilar skull fracture *** · Battles signs, raccoon’s eyes, CSF from nose and ears ottoreah or rhinorrhea (halo signs – blood in middle CSF outside) – take piece of gauze put drop on it and the CSF will go to the outside and blood in the middle. Never put an NG tube because you put it in the brain. o Depressed skull fracture o Comminuted skull fracture · Traumatic Brain Injury Classifications: o Primary ▪ Direct injury to brain · Coup/Countercoup Injury (whiplash) ▪ Types · Concussion o Most common associated with TBI, does not show up on CT, rest the brain. Based on clinical treatment. Only tx: is to rest the brain. · Contusion: Bruise of the brain associated with leaking blood vessels. · Penetrating injuries: Ex: Gun shots · Diffuse axonal injuries: o Most severe, because the axons on neurons get torn 16[Date] Page 16 or stretched (kinda like shaken baby syndrome) · Hematomas o Epidural ▪ Bleeding artery (medical emergency) ▪ Lose consciousness but quickly regain consciousness then dete- riorate quickly 17[Date] Page 17 o Subdural ▪ Bleeding veins ▪ Acute – loss of consciousness, worsening manifestations very quickly. ▪ Chronic subdural seen in the elderly o Intracerebral ▪ Bleeding of brain tissue itself ▪ Trauma or ruptured aneurism ▪ Complications of primary injury · Intracranial bleeding o Secondary ▪ Body’s response to the injury ▪ Consequence of initial trauma · Inflammatory response o Cerebral edema which increases ICP which leads to tissue hypoxia · Release of cytokines o Vasogenic edema · Loss of Autoregulation · Traumatic Brain Injury Management o Nursing (same as increased ICP) ▪ Neurological assessment · Glasgow Coma Scale ▪ Airway assessment ▪ ICP monitoring ▪ Hemodynamic monitoring ▪ Interventions to control elevated ICP ▪ Evaluation of diagnostic tests 20[Date] Page 20 o Large Artery Atherosclerosis – most common o Cardio embolic Events (A-fib) - most common o Small artery occlusion (Lacunar Stroke) o Cryptogenic – unknown cause. Looked at everything no cue reason. · TIA 21[Date] Page 21 o Temporary symptoms then they go away Key*, indicator for stroke later. Do a full workup for patient. · Nursing Managements o Prevention: Most important. ▪ Public education regarding signs/symptoms ▪ Face, Arms(asymmetry), Speech, Time(tongue) “FAST” - sometimes tongue will devil- ate to left or right. o Assessment ▪ History is most important · Time of onset of symptoms for TPA o Time is important because 3-4 hours tape can be administered ▪ Neurological exam · Mental status, cranial nerve function, motor strength, sensory function, ne- elect, coordination ▪ NIH Stroke Scale (table 13-10) valuable tool to evaluate for a stroke, should be used nationwide · Universal, higher score the worse the patient ▪ Airway, breathing, circulation ▪ Hemorrhagic Variations · Localized or worst headache, nuchal rigidity, restlessness/irritability, photo- phobia, nausea and vomiting · Medical Managements o Hemorrhagic Stroke ▪ Goal: MAP < 130 systolic mm Hg (lower side) because you don’t want to increase bleeding. Ischemic patients we want the blood pressure a little higher, but not too high. Greater them 130. ▪ Glycemic management ▪ Diagnostic exams · CT evaluation · Laboratory tests 22[Date] Page 22 ▪ Medications · IV antihypertensive · Manage ICP o Osmotic diuretics ▪ Monitoring for signs of vasospasm 25[Date] Page 25 o Safety precautions/Seizure Precautions Ex: Pads, suction, 02, o Educate patients · Medical Management o Medications: Compliance in taking meds is important, no driving, knowing signs to identify. ▪ Benzodiazepines – drug of choice lorazapam ▪ Anticonvulsants · Dilantin – getting Dilantin level is important · Hereby ▪ Phenobarbital only as last result. CNS Infections - Bacterial Meningitis · A neurological emergency most concerned about · Infection of the pie and arachnoid layers and CSF · Transmission o Blood o CSF contamination during surgical procedures o Skull – direct openings to brain will put you at high risk for meningitis · Clinical Manifestations o Headache, Fever, Photophobia, Petechial Rash on trunk, Nuchal Rigidity – Signs of this: Brzezinski – lift head and knees flex – positive sign Karnack’s sign – flex him and knee and the pt. will feel pain and resistance when straighten leg and sometimes head will lift up (pose- tie) · Diagnostics o Lumbar puncture ▪ CSF will look Cloudy, Lab will fine low glucose because bacteria is eating glucose, high protein, WBCs · Management o Antibiotics, Corticosteroids, Droplet Precautions, Seizure Precautions, Monitor for Increased CP 26[Date] Page 26 Spinal Cord Injury (SCI) · Causes o MVC’s, Falls, GSW, Sport Injuries, Diving Accidents · Primary versus Secondary Injury to the spinal cord o Primary is injury to spinal cord itself o Secondary is body’s response to spinal cord injury 27[Date] Page 27 · Complete Lesion (injury to spinal cord is called lesion) o Total loss below the level of Injury o Movement, sensation, reflexes · Incomplete Lesion o Sparing of some function below the injury o Some function below injury – more common partial loss o Anterior Cord Syndrome o Central Cord Syndrome o Brown-Squared Syndrome · Spinal Shock (or primary injury) o Complete loss below level of injury o This should resolve in maybe a few days or weeks o Resolves when sensation comes back ▪ Motor ▪ Sensory ▪ Reflex activity · Neurogenic Shock (or secondary injury) or system o Disruption of autonomic pathways o SNS shuts down and PNS takes over ▪ Temporary disruption of autonomic pathways below level of injury · Assessment o Airway and ventilation key – make sure we need to protect airway and patient is able to breathe. o KEY: Stabilize spine FIRST o Paralysis of diaphragm and intercostal muscles will result in ineffective breathing patterns ▪ C1 to C3: ventilator dependent ▪ C4 to C5: may or may not need ventilator – Phrenic nerve will be injured which affects diaphragm (breathing) 30[Date] Page 30 ▪ Halo vest ▪ Surgical intervention o Medication ▪ Glucocorticoids – high dose ▪ Vasopressors/fluids 31[Date] Page 31 ▪ Proton pump inhibitors ▪ IV fluids · Thermal Burn o Fluid loss o 90% of cases Burns o Related to time of exposure to very hot or cold objects Ex: fire, stoves, hot eater o Severity of burn is the amount of time you are exposed to the cause. · Chemical injury o Cause protein denaturation (why they are so bad because of break down protein in our tis- sue) o Acids ▪ Cleaning products ▪ Acids stop burning once the agent is removed or flushed from the skin. ▪ You can wipe down the acid and break down of protein will stop. o Bases ▪ Worse than acids ▪ Ex: Oven cleaner ▪ Even after it is removed from skin tissue continues to break down o Organic compounds ▪ Most serious because cause deep tissue denaturation – get to deep layers of skin ▪ Organic compounds can deeply penetrate leading to internal injuries ▪ Ex: Gasoline · Electrical Burns/injury o Internal injury can cause dysrhythmias, you can see spinal cord injury cause it could throw you. o Can cause lethal ventricular fibrillation, central nervous system defects and injuries and titan causing respiratory paralysis. o Burns may not look severe on the outside because the current enters the skin and follows the path of least resistance. Therefore there is a lot of damage underneath the skin that may not be as visible. · Inhalation injuries o 20 to 50% of people who had a thermal 32[Date] Page 32 o Occur after fires or chemical leaks in enclosed spaces. Systemic injury can occur due to toxic gas exposure such as carbon monoxide and cyanide poisoning. o Shallow breathing, pulmonary problems, stridor, o Clinical indications of injury ▪ Facial burns good chance they will have inhalation injury, presence of soot(hash) around mouth and nose, dark tinged sputum, respiratory difficulty o Intervention 35[Date] Page 35 · Bur ns ▪ Arm - 9% each. 4.5 on front 4.5 on back ▪ Torso – 18% - chest 9% - abdomen 9% ▪ Back 18% - 9% upper back – 9% lower back ▪ Legs 18% front and back 9% ▪ Peril area – 1% ▪ Ex: Abdomen B legs = 18, abdomen 9. Lower back 9, front head 4.5 = 40.5 o Hypermetaboloic state b/c your body is trying to heal itself. o At risk for hypovolemic shock o Symptoms same for hypovolemic shock o Patients need a lot of calories to heal (high metabolic state) ▪ High protein · Burn Treatment o Parkland Formula: 4mL x kg(ideal) x TBSA that pt. has been burned – this is how we give fluid back. Ex: 4 mL x 86 x 40 = 13,760 total you will divide by 2 = 6,608mL total you dived in half and the first total you will give in first 8 hours the patient was burned. First 8 hrs. = 860ml/hr. of fluid… the sec- on half of your original total you will give in the first 16 hours. You will set the pump at 430 mills ON EXAM KNOW THIS Ex: 4 m: x 60 x 70 = 16800 … first 8,400 .. 1040 ml/her first then 525 ml/hr. o Resuscitative phase · Within the first 48 hours after the burn ▪ Airway · Early intubation ▪ Breathing · 100% humidified oxygen via face mask or through mechanical ventilation for CO poisoning. ▪ Circulation · Fluid resuscitation using the Parkland Formula · Cardiac monitoring—especially for electrical burns · Patients will still require maintenance fluid that matches urine output. ▪ Neurological Status · Changes in neurological status may indicate potential complications such as seep- sis, hypoxemia, or hypo perfusion ▪ Renal status · Intake and Outtake ▪ GI system · Monitor for ileus or Curling’s ulcer - monitor for stress ulcers and contuse stress ulcer prophylaxis · NGT insertion · Monitor for intraabdominal hypertension (life threatening complication) ▪ Integument system · Main focus is prevention of infection and sepsis · Wound assessments 36[Date] Page 36 · Tetanus immunization · Prevent hypothermia ▪ Monitor blood and electrolytes · Refer to the Laboratory Alert Table on page 640. ▪ Replace patients fluids 37[Date] Page 37 · Parkland Formula o 4ml x kg x % of body burned o Split total in half ▪ First half is given in the first 8 hours ▪ Second half is given over 16 hours · Isotonic fluids – probably lactate ringers o Acute Phase 2nd phase ▪ 48-72 hours after burn- until burn is closed ▪ This phase can last months. ▪ Begins when patient starts to dieresis ▪ Continue interventions of resuscitative phase ▪ 2 greatest concerns · Pain – very painful o IV narcotics o PCA – if alert and aware this is preferred so they can control their pain. · Infection – number 1, huge risk o No skin to protect them ▪ Goes until wound is closed, can last weeks to months. o Rehabilitation Phase ▪ Getting patient as close to function as possible. ▪ Focused Therapy: PT, OT, and social work. A lot of support. ▪ Takes weeks to months o Wound care ▪ Debridement (deep partial and full thickness) ▪ The type of burn will tell the extent and care of the wound. ▪ Removal of old and dead skin with a brush or scrubber. Very painful ▪ Engrafts - pig (animal skins) ▪ Auto grafts – own skin (self) ▪ Synthetic graft ▪ Allografts – cadavers or someone else ▪ Compartment syndrome in wounds that go all the way around arms and legs, or in the abdomen. 6 Ps · Escharotomy to relieve pressure o Concern: Circumferential burns and compartment syndrome from developing swelling and los- ing circulation to skinl ▪ Burns on abdomen can develop abdominal HTN or abdominal compartment syndrome – might need an escharotomy (cut through 40[Date] Page 40 Medical Perennial—correct hypovolemic, positive inotropic agents for decreased cardiac output and treat underlying cause. Intracranial—drug therapy, protein and electrolyte restrict- ton, removal of toxic agents. Post renal—remove the obstruction Treat the cause: Ex: Get perfusion back to kidneys If post renal get rid out of obstruction. Ex: Kidney Pharmacological Diuretics are controversial and it depends on the cause of the failure and can be used to manage fluid overload Dopamine—also controversial – vasoconstriction, vase- presser N-Acetyl cysteine (Mucomyst)—used for patients who are at risk for contrast induced kidney injury. Dose before and after. Give before and after giving contrast dye – it the smelliest! Dosage adjustments Dietary The goal is to provide enough nutrients to maintain homeostasis. Sodium and potassium restrictions. Fluid restriction Hyperkalemia— associated with diastole. Can cause ECG changes that begin with tall peaked T-waves , progressing to a wide QRS complex, flat- toned p wave, to ventricular tachycardia, ventricular fibril- lotion and then cardiac stand- still. Potassium restriction. Dialysis and Kayexalate are the only therapies to reduce potassium levels. Administrate- ton of Kayexalate requires bowel function (bowel sounds). You can give key rectally. Insulin, albuterol and sodium bicarbonate will temporarily push potassium back into the cell. Calcium glucometer will protect the heart from the effects of elevated serum potassium, it doesn’t do anything to potassium it just protects the heart. If giving insulin gives them food/glucose otherwise you will bottom out blood sugar. Potassium is associated with diastole in heart, as potash- sum gets higher it will cause slowing down of heart. Dialysis - if meds do not work you will need this Continuous Renal Replacement Therapy (CRRT) Hemodialysis Peritoneal dialysis (rare) · Dialysis o Vascular access ▪ Catheters · Short term – has arterial port or venous port · Do not touch the catheter! Assess it and nothing else. Assess site make sure its intact. Strictly for dialysis. ▪ Fistula or Graft 41[Date] Page 41 · Long term 42[Date] Page 42 · Hear the Bruit and feel the thrill to check for patency · Avoid arm with fistula or graft for BP, IV, Blood draw, no lab sticks · Even if its old and not working do not use that arm. Do not take blood press- sure till in old one. Take it in the leg. ▪ Monitor labs, weight, vital signs, ▪ Important: Do not want to give meds before depending on what they are. Blood press- sure meds should not be given. Hold anything that will get dialyzed out. Before you should feed patient, weight before, monitor I & O’s. Dialysis Method Nursing Care Complications Continuous Renal Re- placement Therapy— daily- sis that occurs 24/7. It is a lower flow rate for patients who cannot tolerate the fluid shifts of hemodialysis. Run by ICU nurses. Strict monitoring. Hourly intake and output, hourly labs, hypothermia man- agreement, anticoagulation because the filters for CRRT can clot very easily, hourly vital signs (may be more frequent), aseptic technique, prevent kinks and obstructions in the system. Assess access sites. Nurses can operate it. 1 to 1. Hypotension, bleeding/clot- ting, hemolysis, dysrhythmia- miss, infections, hypoxemia, technical errors Hemodialysis—blood is fill- tired through a semipermeable- able membrane where fluid and waste are shifted out of the blood and beneficial moll- clues are reabsorbed Usually performed by dial- yeses nurses or technicians. Monitor lab values, intake/output, daily weights, and monitor vital signs, hold meds that may be dialyzed until after dial- yeses, and assess access sites. Hypotension, bleeding/clot- ting, hemolysis, dysrhythmia- miss, infections, hypoxemia, pyrogenic reactions, dialysate reactions, dialysis disequilibria- rim syndrome, vascular ac- chess dysfunction, technical errors 45[Date] Page 45 stream and cause SIRS and ARDS – can present like septic shock. Mediators can also attach the lungs which causes ARDS. o People can have mild, but severe you will see in the ICU – severe will be very sick. o Clinical manifestations of acute pancreatitis include the following: ▪ Constant Pain (Left upper quadrant) severe and constant ▪ Nausea and vomiting 46[Date] Page 46 ▪ Fever- due to inflammation ▪ * Dehydration/hypovolemic · Volume replacement is key ▪ Abdominal guarding, distention ▪ Grey Turner’s sign—indicates hemorrhage ▪ Cullen’s Sign—indicates hemorrhage o Labs and diagnostic tests ▪ Elevated amylase(HESI), lipase, WBC, glucose (beta cell damage), bilirubin, AST, ALT, LDH, alkaline phosphatase. For HESI amylase is more specific, for textbook it is li- passé. ▪ Amylase and lipase are the most specific indicators. Lipase is more specific than Amy- lase because amylase can be elevated as a result of other conditions. ▪ Decreased calcium, potassium, and albumin. ▪ The hematocrit may be elevated with dehydration but if the patient is bleeding, it can be low as well. ▪ CT scan of the abdomen—detects pancreatic necrosis ▪ MRI—detects pancreatic necrosis ▪ Endoscopic retrograde cholangiopancreatography (ERCP)— combine radiography and endoscopy · Endoscrope dropped down to the duodenum to look at walls of pancreatic ducts. Looking for inflammation. o Treatment ▪ Volume replacement first KEY then pain control, NPO. Rest the pancreas pt. might be on TPN and lipids or patient might get a G- tube. Feeding tubes in jejunum – feeds low so does not stimulate the pancreas. · Viral Hepatitis o Inflammation of the liver o Rest the liver, just symptom management usually. o If chronic he might get antivirals. · Cirrhosis o Failure of the liver o Alcohol the most common cause of cirrhosis. o Early stages: liver gets larger (will be enlarged and inflamed). Compresses portal veins (blood vessel)s feeding the liver which causes portal hypertension. o Later stages: liver starts to shrink and get scarred. o Diagnostic tests ▪ Elevated liver enzymes (ALT, AST), not specific to cirrhosis though ▪ Specific labs to look for Elevated bilirubin and elevated 47[Date] Page 47 ammonia levels (true signs/true labs that patient has cirrhosis) ▪ Changes in coagulation studies o Treatment ▪ Supportive ▪ Treat complications – you need a liver transplant but can treat the complications ▪ Ascites (liver can’t make albumin) respiratory problems.