NUR4050 Final Exam Outline.docx

NUR4050 Final Exam Outline Head Injury: Traumatic Brain Injury: Mechanisms: Acceleration Acceleration-deceleration/Coup-Countercoup Rotational Forces (Most common cause of death during an accident due to axons being sheared from cell bodies) Penetration Pathophysiology: Primary injury: Direct...

NUR4050 Final Exam Outline Head Injury: Traumatic Brain Injury: Mechanisms: Acceleration Acceleration-deceleration/Coup-Countercoup Rotational Forces (Most common cause of death during an accident due to axons being sheared from cell bodies) Penetration Pathophysiology: Primary injury: Direct injury to the parenchyma Hemorrhage and compression of nearby structures Secondary injury: Biochemical and cellular response to initial trauma Can exacerbate primary injury Consequences of increased intracranial pressure Risks of cerebral hypoperfusion Cerebral edema Assessment: ABC’s!! Ensure secure airway. Hypoxia is an independent risk factor for mortality – (Glasgow next slide) Supplemental O2 appropriate for the patient All patients should be monitored w/ pulse ox and frequent checks Maintain MAP >90mmHG with fluids. Another indicator of mortality AVOID DEXTROSE (D5W) Damaging to injured brain All head injuries are C-Spine injury until proven otherwise Glasgow Coma Scale Lowest score you can have is 3, consistent with brain death. Degree of injury and type of injury Mild injury Moderate injury Severe injury Check pupils Fixed and dilated pupils (usually brainstem injury) will have lesions/injury on the same size If one pupil is larger than the other, that usually means the injury occurred on the same side of the larger pupil. Motor Responses to Pain: Assessment of Reversible Causes of MS Changes: D Dextrose 50% (hypoglycemia) O Oxygen 100% (hypoxemia) N Naloxone (Narcotic- pinpoint pupils) T Thiamine w/ fluids (Alcohol withdrawal) (To increase seizure threshold) Additional Assessment: Consider seizure prophylaxis On top of benzodiazepines given for sedation we probably see them on IV Keppra regardless of their history of seizures. Actively seizing IV push Lorazepam and Valium Status Epilepticus Further treatment through intubation and propofol drip. Post-trauma convulsions tx w/ lorazepam Focused physical assessment: Ecchymoses Battle’s sign (retro- auricular bruising/behind ear; suggestive of basilar skull fracture.) Raccoon eyes Facial bone fractures Scalp Lacerations, avulsions (hematoma and fracture together), fractures, hemotympanum (blood behind eardrums), Babinski (Normal= Toes go down) Cranial Nerves: 1-2 Qs on these but not specifics. Reflexes: Sensory stimulus evokes motor response. Cutaneous reflexes graded as normal, abnormal, or absent (ie, plantar reflex) Deep tendon reflexes: biceps, brachioradial, triceps, patellar, and Achilles (Don’t need to know specifics; what matters is the continuum is the patient improving or not. If we do have no response, we should be aware of that). 4+: A very brisk response; evidence of disease, electrolyte imbalance, or both; associated with clonic contractions 3+: A brisk response; possibly indicative of disease 2+: A normal response 1+: A response in the low-normal range 0: No response; possibly evidence of disease or electrolyte imbalance Anatomy of the Brain: Frontal Lobe: Motor function Cognitive functions Judgment. Personality. Reasoning Broca’s Speech Center: Ability to talk and write If someone's speech is impaired that doesn’t necessarily mean they can’t comprehend what's being said. Long term memory Parietal Lobe Sensory interpretation. Temporal Lobe: Hearing Wernicke’s Area Sensory speech Understanding what is said Short Term Memory Hippocampus Occipital Lobe: Visual Brain Optic chiasm transverse across the brain septum so if we have an injury on the left side, we may have pupil dilation on the same side but then vision changes might occur on the other. Cerebellum: Integration of motor function Coordination of movement. Muscle tone Equilibrium (balance) Brainstem: Essential for life Breathing, eating, BP, sexual attraction, reaction Ascending & descending motor & sensory tracts Cranial nerves (all cranial nerves originate here) Reticular formation – arousal Cardiopulmonary regulation Amygdala: Located within the limbic and connects the cortex and brainstem Primarily responsible for memory and relay of info to the cortex May be blunted by constant stimulation from the brainstem. We can stunt our amygdala if were always stimulating it with stressful situations. Ex Normal person, brain hears fireworks, amygdala tells brainstem them its July 4. If it was a miliary person their brain might associate the sound with someone trying to kill them. So, if you're always doing this, you're going to take normal stimuli and react inappropriately to them. Increased Cranial Pressure: Monro-Kellie Hypothesis: Intracranial space has three components Brain substance/parenchyma 80% Cerebrospinal fluid (CSF) 8-12% Blood (3-10%) An increase in volume of one intracranial component must be compensated by a decrease in one or more of the other components This compensation is limited and is influenced by time First things to usually decrease are venous blood and then CSF. Clinical Manifestations: Perfusion: CPP = MAP - ICP (ICP is usually 5-15) (MAP=Mean Atrial Pressure; ICP=Intracranial Pressure; CPP=cerebral perfusion pressure) Reduced CPP is a concern during head injury. As bleeding increases ICP, body will compensate to raise MAP. This way our CPP can stay relatively the same regardless of what the ICP is. Now if we start to decompensate ICP approaches our MAP, it will put pressure on our vagus nerve and cause symptoms below. When beginning to decompensate, symptoms of Cushing’s triad may develop** Widening pulse pressure (1st sign) Decrease Respiratory Rate Decreased Heart Rate If the ICP increases to match the MAP = Bad news; means CPP is 0/No blood supply to brain= Brain Dead. What also happens is that brainstem herniation occurs due to an increase in pressure, and we can only compensate with the brain parenchyma meaning it comes out of the foramen magnum compressing the brainstem which could kill us. Auto Regulation: MAP 50-150 mm Hg no change in CBF Post injury, we want the MAP a bit higher than normal Acidosis, alkalosis and changes in metabolic rate affect CBF Acidosis Hypercapnia = Cerebral vascular dilation Alkalosis Hypocapnia = Cerebral vascular constriction Acidosis conditions cause cerebral vascular dilation (may drop ICP) Hypoxia, hypercapnia, ischemia Hypoxia, hypotension, and intracranial hypertension are the leading causes of cerebral ischemia. Cerebral Edema Types: (Don’t need to know specifics) Vasogenic Edema Disruption in the blood-brain barriers and the inability of the cell walls to control movement of water in and out of the cells. Extracellular fluid in white matter. (We can cause diuresis them easily but harder for intracellular fluid). Brain tumors, cerebral abscess and ischemic and hemorrhagic stroke Cytotoxic Edema Swelling of the individual neurons and endothelial cells, increases fluid in the intracellular space and reduces available extracellular space, affecting the gray matter. Anoxia or hypoxic injury May result in Herniation Management of Brain Injury: Prevent Hypotension and hypoxemia Attempt to maintain a SBP >90mmHg to maintain MAP MAP= (2[DBP]+SBP) / 3 If hypotensive administer 1-2 L of isotonic crystalloid solution immediately. Avoid over hydration as attempts are made to restore adequate blood pressure NEVER D5W Hyperosmolar Therapy/Osmotic diuresis Other than looking for a decrease in ICP you should also look out for their urine output (should increase). GOAL= Increase serum osmolarity to 300-320 –OR- increase serum sodium to 145-150mmol/L Mannitol: Bolus infusion over 10-30 minutes – takes about 20-30 minutes to work Dose 0.25 to 2 g/kg body weight Acts on the loop of Henle to increase the osmotic pull of the collecting ducts Reduces ICP by pulling water from the cerebral parenchymal cells. Hypertonic Agents: Induce hypernatremia to increase cerebral perfusion pressures and decrease ICP. Solutions 3%-23.4% Bolus of 250 ml of 3% Saline will increase serum Na 5 mEq/L Hyperosmolar Therapy = Strict I/O monitoring Respiratory Support: PEEP increases the mean airway pressure and decreases the MAP and CPP Normocapnia (pCO2 35-45) is essential because PaCO2 effects vasoconstriction. Hyperventilation/Hyperoxia: Low PaCO2 increases risk cerebral ischemia by constricting cerebral vasculature Avoid Hyperventilation in first 24 hours First elevate HOB (30 degrees or higher), neck midline, sedation, paralysis, Mannitol, CSF drainage should be tried first. Suction no more than 5-10 seconds, and no more than 2 passes due to coughing because it increases ICP. CNS Depressants: Opioid sedatives help lower ICP by reducing metabolic demand and relieve anxiety and pain. Short-acting opioids are best IV fentanyl: 2-20 mcg/kg over 1-2 min, up to 50mcg/kg, or sufentanil 1-8mcg/kg/min IV Morphine Sulfate for pain Sedatives: Cause little change in CBF, ICP and cerebral metabolic rate Potentiate the effects of analgesic agents Lorazepam, Midazolam in combination with Fentanyl Neuromuscular blocking agents (reduces metabolic demands) Vecuronium or doxacurium Lower ICP and decrease agitation Patient must be sedated and intubated with adequate set rate on vent. Steroids: Decadron Corticosteroids remains controversial Prevents fluid from entering the cells and by increasing blood vessel diameter, thereby promoting cerebral blood flow Decadron in low doses has been shown in rats to decrease brain water content Brain Trauma Foundation guidelines recommend not to use Risk of using outweigh benefits ****Anticonvulsants****: Frequent and routine Neurologic assessment for treatment effectiveness Metabolic needs of paralyzed and non-paralyzed patients increase, administer enteral or parenteral formulas that contain protein w/ dietary consultation Assume spinal cord injury in all head injury patients until ruled out Avoid any condition that increases metabolic rate and increases the demand for O2 and glucose Barbiturate Coma: For severe refractory elevated ICP Last resort to save brain function Ex Phenobarbital given, and it dramatically reduces brain activity. GCS <7, ICP >25 at rest for 10 min, failed maximal interventions including drainage of CSF, mannitol, analgesia, and sedation Use for <72 hours Longer than this it can cause brain injury Need secure airway with mechanical ventilation, continuous monitoring of ICP, BP, cardiac and pulmonary artery monitoring, and continuous EEG monitoring Discontinue if: ICP<15 for 24-72 hours, SBP<90 mmHg with Vasopressors, progressive neurological impairment, &/or Cardiac arrest. Plan is to titrate the barbiturate until the EEG looks flat. Blood Pressure Management: Hypertension Defined as SBP>185 mmHg or DBP 110 mmHg Avoid hypotension and arrhythmias Treat with IV Hydralazine and Labetalol if hypertensive Nicardipine or nitroprusside infusions Need BP continuously monitored by arterial line. Avoid other Calcium channel blockers as they can increase cerebral edema by stimulating vasospasm May use oral beta blockers and ACE-Inhibitors. Monitoring Intracranial Pressure: Monitoring of ICP, CSF drainage and CPP management. Management Intracranial Pressure Monitoring: Brain is contained within inflexible skull, any change in volume is reflected as a change in pressure Monitor changes minute by minute Recommend in any patient with severe brain injury GCS <9 CT scan evidence Bleed or fluid accumulation Types of Monitors: Ventriculostomy Catheter Used the most. Location Ventricle of BRAIN Fiber-optic Specific to area of brain injury; usually for large bleeds. Fluid filled Able to drain CSF fluid Global monitoring Zero and calibrate transducer even small changes are reflected Foramen of Monro is optimal reference point (tragus) Any break or interruption in continuous fluid column will create artifact ICP Waveforms Looks like the reading of an arterial line with a dichotic notch. Our arterial pressures are basically giving us our ICP and subsequent cerebral perfusion, important to understand that. Cerebral Perfusion Pressure (CPP): Blood pressure gradient across the brain Calculated: CPP = MAP−ICP Goal: Range 70-80 Auto-regulatory functions may increase CPP up to 100-120 mm Hg Must be maintained near 80 mmHg to provide adequate blood supply to the brain, but >90mmHg may cause injury CPP <30 mm Hg results in neuronal hypoxia and cell death Normal ICP <20mmHg (usually 5-15; don't want it above 20) Summary of Nursing Implications: Q 1 hr neuro exam: Notify MD immediately for S/S of herniation HOB > 30 degrees, neck neutral position Maintain ICP < 20-25: Decompressive craniectomy, Mannitol, Hypertonic saline Prevent hypoxemia and hypotension Pre-sedate before procedures/care Feed early and advance to goal Attention to fluid & electrolyte balance (changes to pituitary gland) (SIADH/CSW/DI) Treat fever - Tylenol/cooling blankets Because fever increases metabolic demands of the brain. Bowel routine/stool softeners, GI and DVT prophylaxis Due to slowing of peristalsis OT/PT/speech/Rehab consults on day 1 Involve/educate/support family Causes of Brain Abnormalities: Categories: Primary Head Injury: Scalp Laceration: Most common head injury May result in profuse bleeding caused by the great vascular supply to the scalp Monitor for hypovolemia (especially patients on blood thinners) Apply direct pressure to control bleeding First assess for skull fracture Suture/staple laceration after thorough examination and cleansing Lidocaine 1% with epinephrine (local constriction) should be used on scalp lacerations to control bleeding Do not use lidocaine with epinephrine for lacerations on nose or ears Skull Fracture: Simple No displacement of bone. Protect the cervical spine, observe scalp laceration, may indicate underlying brain injury Depressed Bone fragment depressing the thickness of the skull Scalp laceration usually present Asymptomatic or may have altered level of consciousness Surgery is required to elevate and debride the wound Prophylactic broad-spectrum antibiotics Tetanus toxoid if indication Institute seizure precautions (siderails, suction, O2, etc.) Basilar: Fracture in the floor of the skull (can be fatal) Raccoon eyes-periorbital ecchymosis Battle sign-mastoid ecchymosis (behind ear) Otorrhea and/or rhinorrhea (positive dextrostix test, halo or target sign, & salty taste in mouth. Do not obstruct flow) Because outflow of CSF will help the pressure in that vault. Prophylactic antibiotic coverage Oral intubation and oral gastric tube are indicated instead of nasal intubation and nasogastric tube. Because we can perforate the brain if there's a skull fracture. Concussion: Transient, reversible alteration in brain functioning. Brief loss of consciousness amnesia of events. Pathophysiology unclear, thought to be impairment of reticular activating system caused by shearing and impact. Primary concern is an underlying hematoma Lethargy, headache, nausea, dizziness Do not give opioids (masks mental status changes). Evaluate for changes in level of consciousness May need to admit to hospital if unconsciousness lasts longer than 2 minutes or you are vomiting. Diffuse Axonal Injury: Usually results in coma and death High mortality, suspect in any patient with a correlating injury who arrives comatose Deceleration injury coupled with MVC. Results in shearing of axons. Along with hemorrhage and edema Contusion: Bruising to the surface of the brain with varying degrees of edema, coup (Direct) or countercoup (Indirect) injury. Variable LOC, nausea, vomiting, dizziness Visual disturbances Institute seizure precautions Brain stem contusion; Posturing (fencing sign), variable temperature, variable vital signs Hematoma (Explained Below) Infection: Meningitis Spinal tap if we suspect this. Any patient less than 28 days and comes with a fever we suspect meningitis because it is fatal. Brain abscess We have to drain it. Have to be treated with long term antibiotics for both. Brain Swelling or Edema: Secondary to any of the above Brain Injury: Hematomas: Epidural Hematoma Arterial bleeding. KNOW THE HISTORY: Injury followed by lucid period. May last several hours Collection of arterial blood between the skull and the dura mater within the epidural space LOC followed by lucid interval, then rapid deterioration Stupor progresses to coma Ipsilateral pupil dilatation (dilated on same side of injury) Hemiplegia Obtain CT scan Mannitol may be given Immediate surgical intervention is necessary if decreased in neurological function. Small bleeds are monitored. Subdural Hematoma: Venous bleeding between the dura mater and the brain tissue. Requires forceful injury in young patients, elderly patients may develop with less severe injury Most frequently seen type of IC bleeding in the elderly. Acute: Develops over minutes to hours Drowsiness, agitation, confusion HA Unilateral or bilateral pupil dilatation Late hemi paresis Obtain CT scan Surgery is required Chronic: Develops over days or weeks HA Memory loss Personality changes Incontinence Ataxia Obtain CT scan Surgery is usually required, but close monitoring may be sufficient if the hematoma is small Arteriovenous Malformations: When they rupture its similar to a hemorrhagic stroke. Detected: CT scan with and without contrast reveal bleeding sites No contrast if bleeding is suspected. MRI with injection of radioactive reagents 4-vessel cerebral angiogram Treatment: Surgical resection for small-medium size Endovascular Treatment- detachable coils, Onyx liquid Redos-urgery Nursing Care: Admission to ICU Monitor for Neuro changes Hemorrhage prevention Symptom management with BP control Treat pain Prophylactic anti-seizure medication Lifestyle modification No smoking Cerebral Aneurysms: Caused by Atherosclerosis, hypertension, smoking and alcohol consumption also uncontrolled diabetes. Genetic component Symptoms: Headache 3rd nerve palsies (dilated pupils) Extra-ocular motor deficits (Cranial nerve III,IV, VI) Vision changes Pain above and behind the eye Localized HA Nuchal rigidity Seizures Photophobia Severity presentation depends on amount of bleeding: Worst headache of life (thunderclap HA) Nausea Vomiting May or may not lose consciousness Cranial nerve deficits Stiff neck/neck pain Blurred vision HTN, Bradycardia Diagnosis: CT scan without contrast IF negative CT scan for blood-Lumbar puncture for RBC’s and xanthochromia (bile) in CSF CT angiography MRI/angiography Angiograms Treatment: Surgical Clipping Endovascular Techniques Guglielmo coil Stent assisted coiling Nursing Care: Neurological assessment Monitor signs and symptoms of complications: Vasospasm: Begins 3 days after bleed resolves 21 days Hyponatremia: Na<135, due to SIADH, or maybe due to increase loss of Na via urine. Tx with fluid restriction Neurogenic pulmonary edema: Support with Intubation will self-corrected. Cardiac dysfunction: Support with inotropic therapy, pulmonary artery monitoring and vent support. Chronic hydrocephalus Acute Stroke Ischemic: The larger the vessel that’s injured the worse the outcomes. Early recognition and Early treatment Mortality 35%, with 40% of strokes occurring in people under the age of 60 years Leading cause of disability and need for long term care. Risk Factors HTN, smoking, obesity, cardiac disease, hypercholesterolemia, DM, cancer, use of BC pills, and PFO with atrial septal aneurysm. Prevention is anti-coagulation for atrial fibrillation and ASA Treatment: Early recognition (FAST) CT Scan, MRI, Cerebral angiography IV thrombolytic (tPA) administration Intra-arterial within 3 hours from symptom onset Can be pushed to 4.5 hours in some patients 24 hours for intravascular intervention for basilar artery stroke Management: Restoration of CBF Prevent recurrent thrombosis Neuroprotection Supportive care tPA: Given within 4.5 hours or less from onset of last seen functioning normally Patient sleeping and wakes up with signs of stroke won’t get TPA. NIHSS score (measurable defect) and results of imaging will determine if appropriate to give tPA Dose of 0.9mg/kg with (maximum dose of 90mg IV) (don’t need to know dose just know its weight based) 10% bolus over 1-2 minutes; remainder of solution over 60 minutes No other antithrombotic therapy should be given for the next 24 hrs. Major risk is intracranial hemorrhage. Acute Stroke Hemorrhagic: 30-day mortality 40-80%, with 50% of all deaths occurring in first 48 hours. Cause: Aneurysmal AVM Coagulopathies Vasculitis Abuse of cocaine or sympathomimetic drugs Way more N/V with hemorrhagic strokes then ischemic. Trauma: Goals of Trauma Care: Avoid Oxygen supply-demand mismatch Optimize organ perfusion Manage Shock States Obstructive shock management Pneumothorax Cardiac tamponade Cardiogenic shock-MI causes accident, or occurred at time of trauma Hypovolemic shock Within first hour of the injury “Golden hour” Initial time when interventions are most effective in decreasing disabilities and saving lives. With appropriate assessment and treatment most can survive. Early death usually occurs at the scene and happen in the first minutes after the trauma (large-vessel disruption, exsanguinations/catastrophic neurological injuries). First-Responders: Pre-hospital Resuscitation: Immediate stabilization and transportation: Primary survey includes ABC’s Circulation Control of external bleeding and shock Other Considerations: Immobilization (C-Collar) Immediate transport (ground or air) “Right patient to the right resources in the right time frame” Order of Care in Hospital: Primary Survey** Airway, breathing, ventilation, and life-threatening injuries identified. A: Airway Obstruction secondary to maxillofacial injury, chin lift vs head tilt – Are they talking to you? B: Breathing Resp rate, Pulse ox, quick assessment of breath sounds- what would indicate emergent need for treatment? Don’t hear breath sounds on one side? Pneumothorax: They need a chest tube. C: Circulation HR, Blood pressure, pulse check if unresponsive, 2x large bore IVs with fluid/blood products – check distal pulses for injuries D: Disability/Neuro GCS, pupils, limbs (sensation and motor function), glucose level E: Exposure – Expose the patient, complete a head-to-toe assessment Cut clothes off, complete skin assessment APPROPRIATE EXAMS: FAST (Focused Assessment Sonography for Trauma) of chest, abdomen, and pelvis, Portable X-rays. Secondary Survey: Detailed head-to-toe survey, plan for appropriate diagnostic tests. Obtain additional testing as long as patient is stable (CT, MRI, Angiography). A, M, P, L, E: Allergies Medications Past illness/pregnancy Last meal Events/environment related to injury Tertiary Survey: On admission to the ICU, another head-to-toe examination, assess response to interventions, labs and x-rays reviewed. Advanced trauma care after resuscitation (TCAR) Trauma Complications: Acute respiratory distress syndrome Sepsis Shock states Multiple organ dysfunction syndrome (MODS) Renal failure, liver failure, etc. Days and weeks after event will see complications as a result of MODS, and infection. Trauma Care in ICU: ABC Complications of trauma Infection Late presenting injuries Rhabdomyolysis Destruction of skeletal muscles causes increase in myoglobin in blood and can cause kidney failure. Assessment complications of imaging GI Bleeding VAP PE Hypercoagulable state Treatment TBI Managing Trauma: Resuscitation phase: Hypovolemic shock Blood loss Two large-bore peripheral intravenous lines Fluid resuscitation O- until Type and cross is complete Placement of urinary and gastric catheters Fluid Resuscitation: Crystalloids Isotonic, hypotonic & hypertonic. At least 2 liters of isotonic (NS, LR). Colloids Rapid volume expander (albumin, hetastarch) Blood products – FFP, PRBC (If hgb <7 or losing blood proactively) Hemodynamically unstable or are showing signs of tissue hypoxia despite crystalloid infusion Definitive Care/Operative Phase: Trauma is a “surgical disease” Surgical Management: Damage Control Resuscitation: Stage 1 Stop hemorrhage; control contamination and closure methods to close wounds temporarily. Stage 2 Correct physiological abnormalities in the ICU by warming and ensuring adequate resuscitation as well as correcting coagulopathy. Stage 3 Definitive operative management Trauma by Organ System: Musculoskeletal Injuries: Usually not considered life threatening unless there is a traumatic amputation or pelvic fracture Assessment is done in the secondary survey after hemodynamic stabilization** Major causes MVCs, falls, assaults, and industrial, farming, and home accidents Important to understand the circumstances surrounding the mechanism Cervical spine, chest, and pelvis films (x-rays) are obtained first, CT, MRI. Limb swelling, ecchymosis, or deformity is noted, that extremity should be immobilized. Test the extremities for capillary refill (< 2 seconds is normal), pulses, crepitus, muscle spasm, movement, sensation, and pain. Monitor for vascular or neurological compromise. Infection is common with open injuries** Sterile gauze with saline to cover it up. Orthopedic Trauma: Fractures That increase risk of loss of blood Femur Pelvic Watch large amount of blood loss Compartment syndrome Requires emergent fasciotomy Increased pressure in an anatomical compartment results in compression of blood supply. DVT Pulmonary Emboli Fat Emboli Spinal Cord: C3 Area of Diaphragm T6 Sympathetic innervation, if we lose this = Neurogenic Shock. Dermatomes Level of the vertebrae also correlates with skin sensation. Pathophysiology: Result of mechanical forces that disrupt neurologic tissue and/or its vascular supply Primary Injury Occurs at moment of impact. Secondary Injury Comes from the systemic inflammatory response after injury. Complex biochemical processes affecting cellular function Spinal cord ischemia and loss of neurologic function. Immune cells engulf damaged area leading to decreased blood flow and cord ischemia Hypoperfusion of the spinal cord from hemorrhage and edema The release of catecholamines and vasoactive substances decrease circulation and impair cellular perfusion. Neurotransmitters lead to overexcitation of nerve cells. Know that secondary can precipitate a decrease in neurologic function above the primary level of function. Functional Outcome (ON EXAM): Complete Injuries that result in total loss of all sensory and motor function below the level of injury. Tetraplegia Paraplegia Incomplete Recognizable neurological syndromes that are classified according to the area damaged. Brown-Séquard syndrome Central cord syndrome Anterior cord syndrome Posterior cord syndrome Spinal Cord Syndromes (ON EXAM): Central Cord Syndrome Damage greatest to the cervical tract supplying arms; may present with paralyzed arms but with no deficit in the legs or bladder. Brown-Séquard Syndrome Motor paralysis on the same side below the level of the lesion (ipsilateral). Opposite side, below the level of the lesion, there is loss of pain, temperature, and touch Anterior Cord Syndrome Complete motor paralysis below the level of injury (corticospinal tracts) and loss of pain, temperature, and touch sensation (spinothalamic tracts), with preservation of light touch, proprioception, and position sense. Posterior Cord Syndrome Position sense, light touch, and vibratory sense are lost below the level of the injury, while motor function and pain and temperature sensation remain intact. Cauda Equina Damage to s3-s5 Referred to as Saddle Anesthesia Loss of sensory innervation to rectum, perineum and inner thigh Spinal Shock AKA “Shocked” Spinal Cord: Occurs immediately or within hours of an SCI Caused by sudden cessation of impulses from the higher brain centers Loss of motor, sensory, reflex, and autonomic function below the level of injury with flaccid paralysis Loss of bowel and bladder function Loss of temperature control below injury Starts with areflexia, followed by minimal return of reflexes and function As Synapses re-connect, hyperreflexia and spasticity may be present. Neurogenic Shock (Above T6): Form of distributive shock in severe cervical and upper thoracic injury Loss of sympathetic input to the systemic vasculature of the heart; decreased peripheral vascular resistance Hypotension, severe bradycardia, loss of the ability to sweat below the level of injury Orthostatic hypotension: Unable to compensate for changes in position Vasoconstriction message from medulla can’t reach blood vessels because of the cord injury. Maxillofacial Injuries: All I want you to know is that sometimes with these injuries we wire jaws shut and we want to limit the risk of aspiration (from N/V, so Reglan maybe NG tube). So, assess airway clearance. Thoracic Trauma: General: Priority is airway management. Oxygenation and protection from aspiration. Most common causes of airway obstruction are the tongue, avulsed teeth, dentures, secretions, and blood. Injuries to the trachea, thyroid cartilage, or cricoid process Specific Injuries: Chest Wall: Rib fractures Sternal fractures Flail Chest Section or one side of the rib’s sucks in then out. Ruptured diaphragm Significance: Marker for serious intrathoracic and abdominal injuries Sources of significant pain Predictors of pulmonary deterioration Blunt Cardiac Injuries Can’t do much Cardiac contusions-No symptoms to full heart failure and cardiogenic shock Penetrating Cardiac Injuries Cardiac Tamponade Beck’s Triad Decreased BP, muffled heart sounds and increased CVP manifested by elevated JV. Blunt cardiac injuries (BCI) No treatment continue support Pulmonary Injuries or Pleural Space Injuries Pulmonary contusion Tension pneumothorax Most concerning. Penetrating injury on the side of the chest, air fills the cavity and compresses the lung and pushes the mediastinum which occludes the vena cava's causing obstructive/cardiogenic shock. Listen for absent lung sounds Treatment with chest tube. Chest Tubes Bubbling? What does it mean? Occasional bubbling with coughing and movement is normal. Continuous bubbling means air is escaping into pleural cavity around insertion site. We should also see fluctuation in fluid level with each breath. Open pneumothorax Hemothorax Abdominal Injuries: Penetrating Trauma: GSW (ALWAYS require surgery for peritoneal repair), stab wounds Huge risk for infection from translocation of bacteria. Always requires surgery and risk for infection following that. Physical Assessment: Distended abdomen and Rebound tenderness We should never see a distended hard abdomen because it indicates a bowel perforation. Significant peritoneal signs do not show up until later Physical Exam Signs (ON EXAM): Seat Belt Sign Diagonal and lower abdominal abrasion secondary to the restraining belt. May accompany lumbar spine fracture, bowel/bladder perf Cullen’s Sign Periumbilical ecchymoses Hemorrhage in the retroperitoneum Grey-Turners Sign Flank ecchymoses Hemorrhage in the retroperitoneum Kehr’s Sign L shoulder/neck pain associated with spleen injury. Exacerbates with palpation of which quadrant? LUQ Bladder Trauma: Caused by pelvic fractures Know that the pelvis can hide a lot of blood, risk for life threating hemorrhage. Hypermetabolism Initiate enteral feedings within 72 hours for patients with blunt and penetrating abdominal injuries and those with head injuries Renal Complications Renal Failure Rhabdomyolysis can result in myoglobinuria which can then lead to kidney failure. Dark tea-colored urine = Major Sign Burns: Integumentary System: Largest organ Functions: Barrier/protector-Container (maintains status of third space; as the skin keeps that fluid in the body compartment and with burns we lose that) Regulator/Homeostatic mechanism Synthesizer Sensor Acid Mantle: 4.5-6 pH Lipids and organic salts Antibacterial and antifungal properties Depth of Injury: Severity Depends on Duration of contact Temperature of the agent Amount of tissue exposed Ability of the agent and tissue of dissipate the thermal energy Types of Burns: Superficial (1st degree): Epidermis only, painful, red, dry, blanches with pressure, no edema Heal with minimal intervention within 3-5 days Superficial Partial Thickness (2nd degree): Epidermis and superficial dermal layers and heal with minimal intervention in 10-14 days Dermis, moist, pink or mottled red, painful, blisters Deep Partial-Thickness: Entire epidermal layer and deep dermal layers Need surgical intervention if significant in size, and heal 3-4WEEKS Full Thickness (3rd degree): Destruction of epidermis, dermis, sweat glands and hair follicles White, red, brown or black. Reddened areas do not blanche. Require tissue grafting Possible to have no pain in the acute phase Classification of Severity: Minor Burn: Partial thickness <15% BSA in adults and <10% in children Full thickness <2% BSA in adults Moderate, Uncomplicated Burn Injury: Partial thickness 15% to 25% BSA in adults and 10-20% in children Full thickness burns <10% BSA. Major Burns: Partial thickness Second-degree burns of more than>25% BSA in adults or > 20% in children, All third degree (full thickness burns) >10% BSA Burns of hands, face, eyes, ears, feet, perineum, & joints All inhalation burns, electrical burns Burns complicated by fracture or major trauma. Extremes in age, intercurrent diseases. Rule of 9: Pathophysiology: All body systems are affected: Local Response (Primary): Occurs immediately Cellular injury due to heat Release of cellular enzymes – prostaglandin Release of vasoactive substances – Histamines (local vasodilatation), Catecholamines (Raise HR/BP), Platelet activating factor (body doesn’t know it’s a burn), cortisol Activation of compliment (Via Platelet Activating Factor) Altered vascular permeability (via Histamine)(If it results in SIRS, then we would see an increase in vasculature leaking everywhere) Shift of protein molecules, fluid and electrolytes Systemic Response (Secondary): May result in SIRS and infection (septic shock) Greater than 20% of the TBSA will develop a form of hypovolemic shock or burn shock Thermal Injury Systemic Effects: Pulmonary: Increased respiratory rate: Increased Basal Metabolic Rate Increased oxygen demand Decreased Red Blood Cell volume Decreased Hemoglobin Possible Inhalation injury: Closed space injury Assess for: Singed nasal hairs Carbon deposits in sputum (black soot) Facial burns Hoarseness Wheezing Imply tracheal edema which usually gets worse before it gets better. Possible carbon monoxide poisoning Complications: Airway obstruction 24 hrs. Pulmonary edema 24-48 hrs. Pneumonia 48 hrs. and beyond Assess: Work of breathing ABG (carboxy hgb), pulse OX (Carbon monoxide poisoning? Would say 100% because it can't differentiate between oxygen and carbon monoxide) Intubation early Cardiovascular: Catecholamine release-vasoconstriction Massive systemic edema secondary to increased vascular permeability Acid base disequilibrium Anemia secondary to RBC destruction Cardiac output: ½ normal initially then normal within 24 hours (unless patient isn’t treated) Responds to fluid therapy Assess: VS, urine output, weight, CO Renal System: Loss of fluid (pre-renal), increase in K+ (breakdown of RBC), Blood Urea Nitrogen Increases in blood and urine Sluggish glomerular filtration rate Myoglobinuria From muscle destruction, see elevations in Creatinine Kinase. Results in ATN, treated with fluid resuscitation Assess Urine output, BUN, Cr+, CK GI System: Hyper metabolic activity Increased glucose secondary to increased cortisol levels Impaired CHO metabolism Curling’s Stress Ulcer – Specific to burns, resulting from reduced plasma volume, ischemia to GI tract, sloughing of mucosa Assess Bowel sounds, abdominal distention, Blood Glucose Decompress the bowel, add PPI or H2 blocker. Causes of Burns: Thermal: Severity is related to heat intensity and duration of contact Flame, Molten metals, tar, or melted synthetics, Liquid Electrical: Similar to crush injuries; muscle necrosis, rhabdomyolysis, and myoglobinuria Watch for arrhythmia Cervical collar-long bone fractures secondary to muscle contraction Can cause thrombosis of any vessel in the body. Injury not always visible Follow CBC, lyte’s, ECG, urine myoglobin, CPK, cardiac enzymes Chemical Agents – Caustic burns: Severity is related to the type, volume, and concentration and duration Strong acids (found in bathroom cleaners, rust removers) are quickly neutralized or absorbed Rinse off skin and call poison control Alkalis (found in cleaning supplies) cause liquefaction necrosis, may lead to progressive necrosis Radiation Burns: Initially appear hyperemic/red then resemble third degree-Occur days, weeks after exposure If due to medical induced, will occur at entry point of radiation. Usually get worse before getting better. Criteria for Referral to Burn Center Partial-thickness burns more than 10% of TBSA. Children in hospitals w/out qualified personal or equipment for children. Management of Burns: Treatment starts immediately after the burn insult has occurred. Goals: Manage fluids Manage airway Nutritional needs Treatment in the ED: Initial High-flow oxygen Rule out arrhythmia Stabilize in ED, whether patient stays or is transferred. Primary Survey Starts at first contact Airway maintenance with cervical spine protection: First priority Protect airway Cervical precautions if spinal injury suspected Facial burns: suspect inhalation injury Enclosed space: suspect carbon monoxide poisoning Administer 100% oxygen Carbon monoxide binds to hgb with a higher affinity than oxygen. Observe continuously Breathing and ventilation Circulation with hemorrhage control Disability (assess neurological deficit) Exposure (completely undress the patient, but maintain temperature (lose heat from loss of epidermis)) Special Management Considerations: Inhalation injury (leading cause of fire-related death) Clinical signs and symptoms related to central nervous system and heart Delayed Encephalopathy after Carbon Monoxide Poisoning (DEACMP) (Destroys neurons in the brain) Carbon monoxide (CO) poisoning: Normal HbCO is less than 2% 10% No symptoms 20% Headache, nausea/vomiting, dyspnea on exertion 30% confusion, lethargy, tachypnea 40% to 60% Seizure, coma, changes on electrocardiogram >60% Death Tx Methylene blue dye = Prevents neuronal death related to CO poisoning. Burn Care: Thermal: Parkland Formula Fluid resuscitation 1st 24 hours Adults 4ml LR x kg wt. x % burn Children 3ml LR x kg wt. x % burn 1st 8 hours after burn administer ½ of total fluids 2nd 8 hours; administer ¼ of total 3rd 8 hours; administer ¼ of total Lactated ringers usually Second 24 hours after burn: 0.3-0.5 ml x kg x % burn Adults D5W plus potassium and colloid-containing fluid to meet metabolic needs and maintain urinary output Indications of Adequate Fluid Replacement: Urinary output 30-70 ml/hr (0.5 ml/kg/hr) Pulse rate 100-120 pbm CVP <12 cm H2O PAOP <18 mmHg Over 18 = Hypervolemic Lungs Clear Sensorium Clear GI absence of nausea and dynamic ileus Arterial base deficit and lactate normal values Temperature Control Due to loss of epidermal barrier. Acute Phase Diuresis to Wound Healing: Goals: Early wound closure Maintenance of functionality Maintain passive ROM to prevent contractures Prevention of infection Sterile technique Adequate nutrition Pain Management: Burns are very painful (because we are directly injuring nerves) Give intravenous opiates - morphine sulfate and fentanyl Administer benzodiazepines for anxiolysis Do not give intramuscular or subcutaneous pain medications because absorption is unpredictable NO SQ heparin and insulin as well. Administer opioids IV Extremity Pulse Assessment: Edema formation may cause neurovascular compromise Doppler flow probe best way to check arterial pulses Escharotomy may be indicated for circumferential burns of the extremities Will present like compartment syndrome Treatment/Wound Care: Cover with clean, dry dressings or sheets (Vaseline gauze to prevent adherence) Keep patient warm Tetanus prophylaxis for burns greater than 10% TBSA Topical Antimicrobials: Silvadene Silver nitrate Honey Cleaning (make sure there's no heat loss and be gentle) Hydrotherapy Showers Gauze: Xeroform gauze (non-adherent gauze) Debridement: Of the eschar and skin graft closure before eschar becomes infected. Surgical Mechanical (changing dress and tissue comes off) Enzymatic Monitor: Signs of infection Granulation Good sign of wound healing Dressings: Several times per day Functions: Decrease pain Maintain position Keeps wound clean and moist Excision: Done early for deep partial and full thickness Lessen pressure Escharotomy Grafting: Autograft Own tissue Allograft Cadaver Xenograft Tissue from a different organism (tilapia) Maintenance of Function: Position of comfort-position of contractures ROM (Range of Motion) or CPM (Continuous Passive Motion) Splinting and Pressure garments Prevention of Infection: Leading cause of death Sterile technique Isolation (protective) Nutrition Start within 24 hours: Tube feedings start early preventing translocation of bacteria High protein/caloric diet Caloric need maybe 7,000-8,000Kcal/day or less depending on how quickly wounds are surgically closed. Imbalanced nutrition: less than body requirements Up to twice resting caloric requirements Goal is to provide adequate calories to prevent starvation and enhance wound healing Enteral and oral routes preferred. Risk vs. Benefit. Types of Skin Disorders that Act Like Burns: (Hypersensitivity Reactions) Toxic Epidermal Necrolysis (TENS) (Stevens-Johnson’s Syndrome): Most common cause drug reaction Skin sloughs its epidermal layer (usually all of it) High mortality rate 25-50% Treated like burns Staphylococcal Scalded Skin (SSS) (Ritter’s Disease): More frequent in children Reaction to staph infection Low mortality rate 5% Sloughing of skin Treated with antibiotics Endocrine: Neuroendocrine Response to Critical Illness: Severe illness and stress activate hypothalamic-pituitary-adrenal (HPA) axis (T6), resulting in release of Cortisol from adrenal cortex. Acute neuroendocrine response to critical illness: Hypothalamic-pituitary-adrenal axis in acute stress Epinephrine released from medulla of adrenal glands Pituitary Gland: Posterior Release of Antidiuretic hormone (ADH): vasopressin Increase in blood pressure Anterior Growth hormone Corticotropin stimulates release of cortisol Liver and pancreas in acute stress: Glucagon gluconeogenesis and increased blood glucose Thyroid gland in acute stress: Increased levels of T3 and T4**** Adrenal Dysfunction: Causes: Primary hypoadrenalism (Addison’s disease) Lose sodium, bronzing of skin, high potassium. Secondary hypoadrenalism (from the pituitary gland) Critical illness-related corticosteroid insufficiency** Peripheral cortisol resistance Corticosteroid replacement for other conditions followed by abrupt D/C Hyperglycemia: Guidelines related to blood glucose management in critically ill patients Intensive Insulin therapy has been found to be beneficial in patients undergoing Coronary Artery Bypass surgery, but goal glucose levels <100 have led to hypoglycemia Patients with other conditions increased mortality due hypoglycemia Hyperglycemia and the cardiovascular system: Elevated serum glucose levels that remain persistent can worsen HF symptoms Hyperglycemia and brain injury: Hyperglycemia can cause cerebral dehydration due to osmotic diuresis Avoid hypoglycemia Hypoglycemia: Hypoglycemia management Follow protocols D50 Glucose tablets Orange Juice Rule of 15’s 15 grams of rapid acting carbohydrate, wait 15 minutes and check blood glucose. If still low, repeat. Nursing Management: Monitor glycemic side effects of vasopressor therapy (Affects fingerstick) Administer prescribed corticosteroids Monitor blood glucose and insulin effectiveness Provide nutrition Maintain surveillance for complications Patient and family education Diabetes Mellitus: Diabetes mellitus (DM) = Carbohydrate intolerance and insulin dysregulation Diagnosis: A1C > 6.5% or Fasting plasma glucose = 126 mg/dL or Two-hour plasma glucose level 200 mg/dL or more during an oral GTT. or Patients with classic symptoms of hyperglycemia or hyperglycemic crisis, random plasma glucose level of 200 mg/dL or more Types of Diabetes: Type 1 Beta-cell destruction, usually leading to absolute insulin deficiency. B cells no longer secrete insulin Autoimmune disease Diabetic ketoacidosis (DKA) may be first manifestation of disease for children and adolescents Management of type 1 diabetes IV or subcutaneous insulin Insulin is required to keep T1DM patients alive They require: Basal (continuously acting insulin) to control glucose levels that would otherwise increase secondary to glycogenolysis (release of glycogen) by the liver Insulin pump basal rates (inject continuously, 24/7 once programed), long-acting insulin (Lantus, Levemir) Bolus (single doses) to control carbohydrate intake and subsequent glucose release into the bloodstream Insulin pump bolus (Programmed by user before meals), NovoLog/Humalog injections in non-pump users Type 2 Progressive insulin secretory defect in addition to insulin resistance. Majority of patients are adults, but with increasing child obesity we are seeing increase incident in children Associated with metabolic syndrome Imbalance between insulin production and use Inadequate insulin response versus insulin resistance syndrome or combination of both Glycated Hemoglobin (A1C; over past 3 months): Diabetic Target Less than 7% Pregnant 6.5% Over 80 8% Diabetic Ketoacidosis (DKA): Epidemiology/Etiology: Life-threatening complication of DM Typically affects patients with type 1 diabetes but can affect patients with type 2 diabetes. Absolute Insulin deficiency Manifests with severe hyperglycemia, metabolic acidosis & fluid and electrolyte imbalances Elevation of counter-regulatory hormones GH, cortisol, epinephrine and glucagon Pathophysiology: Insulin deficiency Leads to disordered metabolism of proteins, carbohydrates and fats Concomitant elevation of counter-regulatory hormones such as growth hormone, Cortisol, epinephrine and glucagon exacerbates the condition of elevated glucose levels Hyperglycemia Fluid volume deficit Hypovolemia Ketoacidosis Acid-base balance Diagnostic Criteria: Blood glucose < 500 mg/dL Metabolic Acidosis from accumulation of ketoacids- pH below 7.3 Serum bicarbonate below 15 mEq/L Moderate or severe ketonemia or ketonuria Hyperosmolality from hyperglycemia and dehydration Volume depletion from osmotic diuresis Causes: Infection Inadequate Insulin therapy Severe illness (CVA, MI, pancreatitis) Alcohol abuse Trauma Drugs Sudden discontinuation of insulin Present in DKA with initial diagnosis DM Type 1 Some Type 2 Diabetics can develop in catabolic stress associated with severe critical illness. Assessment and Diagnosis: Clinical Manifestations: Malaise Headache Polyuria Polydipsia Polyphagia Nausea and vomiting Extreme fatigue Dehydration Weight loss Central nervous system depression and decreased level of consciousness, stupor Coma Dehydration Flushed, dry skin Tachycardia Hypotension Kussmaul’s respirations Fruity odor of acetone Lab Values: Anion Gap: 20+ (metabolic acidosis) Elevated Glucose Ketones in blood and urine Hypercholesterolemia may be present Hypertriglyceridemia may be present Hyperamylasemia (amylase) may be present Treatment: Hypovolemia most acute and critical problem Replace fluids with 0.9NS at 1000ml/hr for 1-2hours 0.9 NS (low Na) at 250-500 ml/hour to correct fluid deficit 4-8L deficit depending on hydration state As soon as serum BS drops to 200 change fluid to D5/.45NS to prevent cerebral edema and hypoglycemia at 150-250 ml/hr Expect 4-8L in first 24 hours Administer IV KCL 20-30meq/liter of fluid in first 2-3 hours of therapy unless potassium levels exceed 5.0mEq/L. Maintain K+ between 4-5 mEq/L If K+ is < 3.3, hold insulin and give KCL until K>3.3. Monitor other electrolytes Insulin Therapy: Start initial IVP of 0.1unit/kg of REGULAR INSULIN Then IV infusion 0.1-0.2 units/kg/hr (don’t need to know the rate just know it’s a lot. Also, IV insulin has a very short half-life) Expected BS drop of 50-75dL/hr, expect drop of 10% When plasma glucose <200-250 mg/dL decrease infusion to decrease insulin until DKA Resolves *Alternatively, a long-acting insulin will allow the drip to come off* NaHCO3 Replacement rarely needed and may be used if pH <6.9, but stop once pH reaches > 7.0 Most often ordered as a bicarbonate drip as opposed to IVP Medical Management Goals: Reverse dehydration Replace insulin Reverse ketoacidosis Replenish electrolytes Nursing Management: Administer fluids, insulin, and electrolytes Monitor response to therapy Surveillance for complications Fluid overload Hypoglycemia Hypokalemia/hyperkalemia Hyponatremia Risk for cerebral edema*** (if glucose is dropped to fast) Risk for infection Patient and family education For every 1pt of A1C above 3 it increases your chances of an MI by 20% Hyperglycemic Hyperosmolar State/Hyperglycemic Hyperosmotic Non-ketotic State (HHS): Epidemiology/Etiology: Potentially lethal complication of type 2 DM Hallmarks: *Extremely* high levels of plasma glucose No acidosis Elevation in hyperosmolarity causing osmotic diuresis and dehydration Differences between HHS and DKA: Extremely elevated serum glucose levels 600+ More profound dehydration Minimal or absent ketosis Proteins and fats are not used for glucose HHS does not develop in patients with type 1 diabetes Pathophysiology: Deficit of insulin (not absolute) Excess of glucagon Results in: Hemo-concentration Hypovolemia Dehydration Risk for Thromboemboli Incidence/Predisposing Factors: Recent onset of T2 diabetes Receiving TPN or high-caloric feedings Infection also major risk factor. Medications: Thiazide diuretics, steroids, hypertonic solution Illness, trauma, or stress Diet-controlled diabetes Pancreatitis Increased incidence in diabetic patients of advanced age Assessment and Diagnosis: Clinical Manifestations: Slow, subtle onset Initial symptoms are nonspecific Marked fatigue/malaise, confusion, S/S of dehydration Physical examination findings Very elevated glucose levels Laboratory Studies: Blood glucose level greater than 600 mg/dL Serum osmolality greater than 320 mOsm/kg Acidosis usually absent (unless hypovolemic shock state not due to ketones) Elevated hematocrit level Decreased potassium and phosphorus levels Increase blood urea nitrogen/creatinine ratio (mimicking pre-renal failure state) Absent ketones Treatment: Medical Rehydration Insulin administration to facilitate the cellular use of glucose Insulin treatment usually less then DKA: Initial bolus of 0.1-0.15 units/kg IV followed by 1-2 units/hours titrated until BG levels are acceptable OR 0.1 units/kg per hour to achieve a decrease of serum glucose of 50-75 mg/dl per hour Electrolyte replacement Nursing Management: Administration of fluids, insulin, and electrolytes Monitor response to therapy Surveillance for complications Monitor for signs of infection Patient education Collaborative management Anticoagulation for DKA/HHS: Increase risk for thrombosis Prophylactic heparin administration should be considered unless contraindicated. At risk for DIC Diabetes Insipidus: Etiology: Insufficiency or hypofunction of antidiuretic hormone (ADH)- made in the hypothalamus, stored and released from pituitary ADH stimulates kidney tubules to be permeable to water so that water is reabsorbed back into the bloodstream Inadequate ADH means that large quantities of dilute urine are passed Three Types: Central DI Pituitary gland issue Nephrogenic DI. Loss via kidneys Psychogenic DI Excessive drinking causing excessive urination Pathophysiology: Free water excreted in urine Extracellular dehydration Hypotension Hypovolemic shock Decreased cerebral perfusion Polyuria Serum Hypernatremia (unless it is psychogenic- then you’ll see hyponatremia) Assessment and Diagnosis: Clinical Manifestations: Dramatic increase in dilute urine output Absence of diuretics, fluid challenge, or hyperglycemia Laboratory Studies: Serum sodium level greater than 145 mEq/L. (Unless psychogenic) Serum osmolality greater than 295 mOsm/kg water Urine osmolality less than 300 mOsm/kg water Medical Management: Volume restoration Medications Medications used for central DI Vasopressin (Pitressin) Medications used for nephrogenic DI Hydrochlorothiazide Nursing Management: Administration of fluids and medications Evaluation of response to therapy Surveillance for complications Patient education Collaborative management Syndrome of Inappropriate ADH (SIADH): Opposite of DI Excess Anti-Diuretic Hormone (ADH) Kidneys reabsorb too much water Dilutional hyponatremia Etiology: Head or central nervous system injury Trauma, anoxia Malignancy Positive end-expiratory pressure with mechanical ventilation Causes low-flow states due to pressure on pulmonary arteries making the brain think more fluids are needed. Pathophysiology: ADH released by posterior pituitary gland ADH regulates water and electrolyte balance Excessive ADH Over-hydration Low sodium (dilutional) Concentrated urine Assessment and Diagnosis: Clinical Manifestations Clinical presentation in SIADH relates to water and sodium imbalance Lethargy Anorexia Mental confusion Seizures, coma, death Laboratory Values: Serum laboratory values Serum osmolality Serum sodium Urine laboratory values Urine osmolality (concentrated) Urine sodium (high) Urine specific gravity (high) Medical Management: Fluid restriction Sodium replacement – only when it gets critically low Around 130 may restrict fluids Around 120 we start to get worried and want to replace it Medications: Stop drugs that may cause SIADH Medications that increase renal water excretion Demeclocycline Vasopressin receptor antagonists Conivaptin Goal of Treatment: Reasonable correction parameters consist of a maximal rate of correction of serum sodium in the range of 1–2mEq/L per h as long as the total magnitude of correction does not exceed 25 mEq/L over the first 48 h. (a) the patient‘s symptoms are abolished, (b) a safe serum sodium (generally 120 mEq/L) is achieved, or (c) a total magnitude of correction of 20 mEq/L is achieved Replacement rates beyond the recommendations result in ’osmotic demyelination’ (Central Pontine Myelinolysis/CPM) resulting in spastic quadriplegia and delirium Irreversible Nursing Management: Restriction of fluids Surveillance for complications Patient education Collaborative management Summary of Endocrine Disorders: Hyperthyroidism Thyroid Storm: Etiology: Excessive uptake of thyroid hormone Increased metabolic activity Sympathetic nervous system response Risk Factors: In the Presence of a Known Preexisting Condition Hx of graves disease Hx of nodular Goiter Thyroid adenoma Precipitating factors: Infection Trauma Stress Coexistent medical illness (MI, Pulmonary disease) Pregnancy Exposure to cold Hyperthyroidism Thyroid Storm Pathophysiology Sympathetic overload Increased metabolic rate: Febrile, Diaphoretic, agitated, nervous, tremulous, abdominal cramping/pain/weight loss Tachycardia, high blood pressure (Wide pulse pressure), fever, agitation --> delirium Increased cellular oxygen consumption Metabolic acidosis Hypersensitivity to increased adrenergic-binding sites Beta Blockers Exophthalmos Can be permanent. Assessment and Diagnosis: Combination of PMH and current clinical manifestations Laboratory Findings: The TSH level will be LOW due to feedback system being altered by the high amount of hormone in the system. Total T4, free T3 & free T 4 elevated Serum calcium levels are decreased if Calcitonin release is suppressing osteoclastic activity Hyperglycemia from insulin resistant. Medical Management: 1 Treat precipitating factor or factors 2 Block excessive thyroid hormone release 3 Block the conversion of T4 into T3 (peripheral conversion) T4 starts and then circulates in the body and becomes T3 which is more potent. 4 Block the peripheral (Sympathetic) effects of thyroid hormone Medications: 1. Thionamides Block production/Release of T4, prevent peripheral conversion T4-T3 PTU (Propylthiouracil) MMI (Methimazole) 2. Iodine Must be given 1 hr. AFTER administration of thionamides to prevent peripheral conversion Potassium Iodide Lugol’s solution Lithium Carbonate 3. B-Blockers Blocks sympathetic effects of thyroid storm Propranolol/Esmolol 4. Steroids Blocks peripheral conversion of T4/T3 Hydrocortisone Nursing Management: Hyperkinesis/Agitation Benzodiazepine Hyperthermia Cooling blanket and antipyretic (Tylenol, not ASA) Rehydration Fluid replacement therapy Electrolytes Nutritional needs are elevated Patient education Collaborative management Hypothyroid Myxedema Coma: Hypothyroidism Severe deficiency or absence of thyroid hormone Myxedema Coma Severe hypothyroidism Etiology: Deficiency of circulating thyroid hormone Decreased metabolic rate and mental status change Often associated with other conditions Afflicts elderly more commonly Symptoms: Depression Weight gain HYPO- Thermia Glycemia Natremia Ventilation Hx of Thyroid surgery, radio ablative surgery, previously on thyroid hormone Laboratory Studies: Low T4 Elevated TSH levels Pharmacologic Management: Levothyroxine or thyroid hormone-Levels should increase slowly IV -T4 500 mcg initially IV –T4 75-100 mcg daily OR IV-T3 25 mcg every 8 hours for the first 24-48 hours Glucocorticoids (Hydrocortisone) Impaired adrenal function seen with profound hypothyroidism Fluid replacement/Electrolyte replacement (Correct Hyponatremia) Re-warm with blankets Monitor LOC Nursing Management: Pulmonary care Cardiac concerns Thermoregulation Thyroid replacement therapy Synthroid should be taken on an empty stomach in the morning with 8oz of water then wait 1 hr before eating anything else. Skin care Elimination Patient education Collaborative management Organ Transplant: 85,000 individuals are waiting for organs, with kidney the most sought (58,000) (Due to high incidence of HTN, diabetes and because you can live for a long time without functioning kidneys) Types of Donors: Deceased Donor: Brain dead or neurological death donor – Most viable donor Traumatic brain injury, anoxic death Non-heart-beating donor – Lesser viability – Living donor Related (parent or sibling) Unrelated (spouse or friend) Paired exchange Two-way exchange occurs Altruistic Registry Terms: Graft Refers to the organ that was transplanted Allograft Non-self of same species Autograft Self Living Donor Donor is alive when giving organ to recipient, may be relative, friend or anonymous Liver, kidneys, bone marrow are big ones. Donor Person who gave organ Recipient Person receiving organ Calcineurin Chemical responsible for activation of T-cell Inhibitors include Tacrolimus and Cyclosporine T-cells Responsible for cell-mediated response B-cells Responsible for humoral response (anti-body production) HLA (H