Shock Types PDF

Chapter 11 shock Shock : a physiological state of systemic reduction in tissue perfusion which results in decreased tissue oxygen delivery and insufficient removal of cellular metabolic products resulting in tissue injury - Shock is a loss of homeostasis - Increased oxygen demand and...

Chapter 11 shock Shock : a physiological state of systemic reduction in tissue perfusion which results in decreased tissue oxygen delivery and insufficient removal of cellular metabolic products resulting in tissue injury - Shock is a loss of homeostasis - Increased oxygen demand and decreased oxygen supply Anaphylactic shock Severe allergic reaction to any antigen, examples are drugs, IVP dyes, blood products, seafood, or nuts What happens in anaphylactic shock Both veins and arteries vasodilate, leading to decreased blood returning to the heart Capillaries become more permeable causing massive interstitial edema Anaphylactic shock physical findings Edema Blood vessel dilation Bronchospasms Fluid shifts ○ All due to allergic reactions to antigens Signs and symptoms anaphylactic shock Pale cool skin Hypotension Respiratory distress Edema rash Treatment of anaphylactic shock Epinephrine Corticosteroids Antihistamines IV fluids Oxygen Neurogenic shock Loss of sympathetic control of resistance vessels that cause a massive venous and arterial vasodilation What happens with Neurogenic shock Venous side: blood pools causing stroke volume, cardiac output, and Blood pressure to fall Arterial side : decreased peripheral Vascular resistance Neurogenic shock patho and causes Severe vasodilation due to anesthesia or spinal cord disorder Neurogenic shock signs and symptoms Skin is pale and warm Bounding pulse Bradycardia Hypotension Neurogenic shock treatment IV fluids Oxygen Vasopressors Lying flat Hypovolemic shock Blood/fluids have left the body causing a decreased amount of volume Bottom line inadequate tissue perfusion Pathophysiology Hypovolemic shock Reduced venous return Reduced ventricular filling ( diastole ) Decreased cardiac output Tissue anoxia Metabolic acidosis Causes of hypovolemic shock Acute blood loss Intestinal obstruction Burns Peritonitis Acute pancreatitis Dehydration Signs and symptoms hypovolemic shock  Pale cool and clammy skin Decreased level of consciousness Rapid shallow respirations Urine output less than 0.5ml/kg/hour Rapid thready pulse map< 60 mmhg Hypovolemic shock treatments Prompt and vigorous blood and fluid replacement Positive intropics : Dopamine, norepinephrine, dobutamine Septic shock Systemic response to infection that is affecting multiple organs What happens in septic shock immune/inflammatory response is not adequate to treat the infection and actually causes more damage Patho and cause of septic shock Patho: release of chemical mediators in response to invading organisms Cause: Gram negative bacteria, Gram positive bacteria, or fungal infection Signs and symptoms septic shock Early signs and symptoms Pink flushed skin Rapid respirations Bounding pulse Normal to slightly elevated BP Late signs of septic shock Skin is pale and cyanotic Rapid respirations Thready pulse Hypotension Treatment of septic shock Antimicrobials Colloids or crystalloids Oxygen  Diuretics Vasopressors Significant labs Increased lactic acid Cardiogenic shock Inadequate myocardial contractility What happens in Cardiogenic shock The left ventricle has been injured leading to impaired pumping Patho cand causes of cardiogenic shock Decreased cardiac output, left ventricular dysfunction, and myocardial ischemia due to Acute MI, myocarditis, papillary muscle dysfunction, or ventricular dysfunction Signs and symptoms of cardiogenic shock Pale cool clammy skin Decreased LOC Rapid thready pulse Rapid shallow respirations Map < 60 mmhg S3 gallop rhythm Faint heart sounds Treatment of cardiogenic shock Vasopressors Intropics Vasoconstriction Osmotic diuretic Oxygen Intra arterial BP ( A line) Obstructive shock **** Life threatening *** Anatomical obstruction in the vessels of the heart leading to decreased venous return and cardiac output with increased after load  Causes of obstructive shock Significant pulmonary embolism Severe pulmonary hypertension Pneumothorax Pericardial tamponade Restrictive cardiomyopathy Constrictive pericarditis Signs and symptoms of obstructive shock Respiratory distress Tachycardia Hypotension Tachypnea Air hunger Chest pain Dilated engorged neck veins Treatment of obstructive shock Cardiac cath ( remove the embolism ) Valve replacement sug=rgeries Dissolving clot Pericardiocentesis Pericardiectomy Shock Practice NCLEX questions NCLEX questions on Shock Flashcards | Quizlet  Chapter 60 CNS Brain and spinal cord PNS Cranial and spinal nerves ANS SNS Neuron The basic functional unit Function of the nervous system Controls all motor, sensory, autonomic, cognitive, and behavioral functions Neurotransmitters Communicate messages from one neuron to another or a specific target tissue Many neurologic disorders are caused by an imbalance in neurotransmitters ie: depression and lack of dopamine Bones and sutures of the skull The bones are put together by INFLEXIBLE jointing points, fused together, and very tightly fitted to one another What are the meninges A protective connective tissue that are around the brain and spinal cord Three spaces in the meninges Pia mater Arachnoid mater Dura mater The circle of Willis Circle around the center above the brainstem with branching arteries, it functions as a roundabout for the two major arteries in the brain,, supplies blood to the brain both posteriorly and anteriorly, is essential for blood flow, minimizing the effects of stroke ○ A complete circle of Willis functions as a fail-safe. If one of these two blood vessel pathways becomes damaged, such as from a ruptured brain aneurysm or stroke, the other pathway can still provide blood flow to the affected part of your brain via the CoW. The cranial Nerves Olfactory Nerve CN1 ○ Provides sense of smell Optic nerve CNII  ○ Provides vision Oculomotor nerve III ○ Opening and moving of your eyes and adjusting pupil width Trochlear Nerve CN IV ○ Looking down and moving yours eyes toward and away from your nose Trigeminal nerve CNV ○ Providing sensations in your eyes, most of your face, and inside of your mouth, allows you to chew food Abducens Nerve CN VI ○ Moving your eyes from left to right Facial Nerve CN VII ○ Facial expressions, providing sense of taste in parts of your tongue Vestibulocochlear nerve CN VIII ○ Provides sense of hearing and balance Glossopharyngeal Nerve CN IX ○ Taste sensations on part of your tongue, swallowing muscles, BP regulation, Saliva production Vagus nerve CN X ○ Regulates several automatic functions such as : Digestion Heart rate Breathing Mood Saliva production PNS Accessory Nerve CN XI ○ Shoulder and neck movement Hypoglossal nerve CN XII ○ Tongue movement when talking, eating, swallowing Cranial nerves location Olfactory and optic are in the cerebrum Other 10 are in the brainstem Dermatome Distribution The body's surfaces that directly relate to a place in the spinal cord If you have an injury at T4 your body will be affected at that point and lower Injury at C3 means no life Autonomic nervous system Regulates activities of internal organs Maintains and restores homeostasis SNS : fight or flight ○ Main neurotransmitter is norepinephrine PNS: rest and digest Neuro Assessment : health history Pain Seizures Dizziness Vertigo Visual disturbances Weakness Abnormal sensations Past health, family, and social history Neuro assessment Conscious and cognition ○ Mental status ○ Intellectual function ○ Thought content ○ Emotional status ○ Language ability ○ Impact on lifestyle Cranial nerve checks ○ Motor system Muscle size, tone and strength Coordination and balance Romberg test ○ Sensory system Tactile sensation Superficial pain Temperature Vibration Position sense ○ Reflexes DTRs Biceps Triceps Brachioradialis Superficial  Pathologic Plantar ( babinski ) Gerontologic considerations Know the difference between normal and abnormal aging ○ Structural and physiologic changes ○ Motor and sensory alterations ○ Temp regulation and pain perception Distinguish delirium from dementia Chapter 61 Altered level of consciousness Level of responsiveness and consciousness is the most important indicator of the patient's condition ○ Level of consciousness : continuum form normal alertness and full cognition to coma ○ Coma : unconsciousness, unarousable, unresponsive ○ Akinetic mutism : unresponsiveness to the environment makes no movement or sound but sometimes opens eyes ○ Persistent vegetative state: devoid of cognitive function but has sleep wake cycles ○ Locked in syndrome: in ability to move or respond except for eye movements due to a lesion affecting the pons Level of consciousness Confused : disoriented to surroundings, likely impaired judgment, may need cues to respond to commands Lethargic : Drowsy, needs gentle verbal or touch stimulation to initiate response Obtunded : responds slowly to external stimuli, and needs repeated stimulation to maintain attention and response Stuporous: Responds only minimally with vigorous stimulation may only moan as verbal response Comatose: No observable response to any external stimuli Signs of diminished level of consciousness Earliest signs ○ Inattention ○ Mild confusion ○ disorientation ○ Blunted responsiveness Late signs ○ Patient becomes markedly inattentive and variably lethargic and agitated ○ Patient may progress to obtunded and may respond to only vigorous or noxious stimuli Assessment of the patient with altered level of consciousness Verbal response Alertness Motor response ( posturing ) Respiratory status  Eye signs Reflexes Glascow Coma Scale Assess patients level of arousal Measures patients basic brain functions of the cerebral cortex and brainstem Records best response to ○ Eye opening ○ Verbal response ○ Motor response Max score is 15 and minimal score is 3 Used for TBI or hypoxic events Ratings ○ Mild 13-15 LOC30 minutes Physical or cognitive impairments ( may resolve ) Consider some rehabilitation ○ Severe disability 3-8 Coma unconscious state No meaningful response no voluntary activities Pupil reactions Anisocoria ○ One pupil dilated Miosis ○ Both pupils constricted Mydriasis ○ Both pupils dilated Dolls eye movement If the comatose patient’s brainstem is intact, when the head is turned in one direction, the eyes move to the opposite side, like a doll’s eyes. If the eyes continue to look straight (stay midline) without movement relative to the head position, this is negative for the doll's eye movements and may indicate a lesion of the midbrain or pons. This reflex is suppressed in a conscious adult with normal neurologic function but is active in a comatose patient with brainstem function. Abnormal Posturing Decebrate : ○ (Extension )indicates upper brain damage, arms are adducted and extended, with wrists pronated and fingers flexed, legs are stiff extended with plantar flexion of feet and internal shoulder rotation ○ Indicates lesion in the forebrain pons Decorticate : ○ ( flexion ) Indicates damage to one or both of the corticospinal tracts, the arms are adducted and flexed, with wrists and fingers flexed on the chest, the legs are stiffly extended and internally rotated. Elbow flexion and shoulder adduction ○ Indicates the brain stem is no longer functioning Potential complications TBI Respiratory failure or distress Pneumonia Aspiration Pressure ulcer DVT Contractures First priority in plan of care in patient with altered level of consciousness Obtain and maintain patent airway ○ Oral or nasal intubation or tracheostomy ○ Mechanical ventilation used to maintain adequate oxygenation and ventilation until ability to breathe is determined Plan of care patient with altered level of consciousness Obtain and maintain patent airway Monitor circulatory status to ensure adequate perfusion Insert IV for Iv fluids and medication access FT or GT initiated ASAP Treat the underlying cause Nursing Interventions: patient with altered level of consciousness Maintain patient airway ○ Monitor respiratory status frequently ○ Position to promote drainage of secretions ○ HOB elevated 30*, lateral or semi prone positions ○ Suctioning oral hygiene chest PT Protect the patient ○ Frequent skin checks ○ Turning schedule ○ Positioning in correct body alignment  ○ Passive ROM ○ Clean eyes with NS on cotton balls ○ RX artificial tears ○ Eye patches cautiously ○ Oral care ○ Speak to patient Maintain fluid status ○ Admin SLOW IV fluids ○ Assess tissue turgor, mucosa, CMP, and I+O ○ Tube feeds Maintain body temperature ○ Monitor temp frequently ○ Adjust environment and cover patient appropriately ○ If temp is HIGH use minimal bedding, acetaminophen, hypothermia blanket, give cooling sponge bath, use a fan ○ If temp is LOW use warming blanket, if shivering use meperidine Promote bowel and bladder function ○ Assess for urinary retention and incontinence ○ Catheter, purewick ○ Bladder program ○ Assess for abdominal distention, and bowel sounds ○ Promote elimination ie stool softeners Sensory and stimulation ○ Talk to and touch the patient ○ Maintain day night sleep wake cycles ○ Limit stimuli when patient is arousing from a coma Increased intracranial pressure Monro kellie hypothesis : ○ Due to the limited space in the skull, an increase in any one of the components of the skull ( brain tissue, blood, CSF) will cause a change in volume in the others Compensation ro maintain a normal ICP of 10-20 mmhg is normally accomplished by shifting or displacing CSF Increased ICP decreased cerebral perfusion and causes ischemia, cell death, and further edema If the ICP gets high enough it may shift through the dura causing HERNIATION ○ Herniation : excess pressure has caused things to get twisted and turned Autoregulation : refers to the brain's ability to change the diameter of blood vessels to maintain cerebral blood flow (compensation ) CO2: decreased CO2 results in vasoconstriction and increased CO2 results in vasodilation Cerebral Perfusion Pressure Closely linked to ICP Map-ICP= CPP  Normal CCp is 70-100 A CCP less than 50 results in permanent neurologic damage Ischemia and Vasodilation Reduced CPP leads to increased ischemic, vasodilation, increased intracranial pressure and further reductions in CPP leading to further neurologic injury Decreased Cerebral blood flow patho overview Increased ICP decreases cerebral blood flow leading to cell death and ischemia ○ Signs include: Rising blood pressure Slow, bounding pulse Irregular Respirations Increased PCO2 = vasodilation ( increasing blood flow and ICP) Decreased PCO2= vasoconstriction ( decreases blood flow) Cerebral edema Patho overview Abnormal fluids accumulation in the intracellular, extracellular or both leading to an increase in brain tissue volume ○ Signs include: Headaches N/V Lethargy Cranial Neuropathy Altered mental status Coma Death Signs of increased ICP Early signs of increased ICP ○ Changes in LOC ○ Sudden change in condition Restlessness, confusion, increasing drowsiness, increased respiratory effort, jerky purposeless movements ○ Pupillary changes and impaired ocular movements ○ Weakness in one extremity or one side ○ Headache : constant, increasing in intensity, or aggravated by movement or straining Late signs of increased ICP ○ Respiratory and Vasomotor changes ○ VS: increased systolic blood pressure, widening pulse pressure, and slowing heart rate, may fluctuate rapidly from bradycardia and tachycardia, temperature increases Cushing's triad: Bradycardia, hypertension, bradypnea ○ Projectile vomiting ○ Further deterioration in LOC ○ hemiplegia , decortication, decerebration, or flaccidity  ○ Respiratory pattern alterations including cheyne stokes breathing and arrest ○ Loss of brain stem reflexes : pupil, gag, corneal and swallowing Assessment of patient with increased ICP Obtain history of events leading to illness Evaluate mental status, LOC ( glascow coma scale, neuro checks ) Assessment of selected cranial nerves Assess cerebellar function, reflexes, motor and sensory function Pupil checks Frequent vital signs Q15 minutes Assessment of intracranial pressure GOLD standard ICP monitoring Monitor it directly through intraventricular catheter, intraparenchymal sensor hooked up to monitor Collaborative problems and potential complications Brainstem herniation : excessive increase in ICP, pressure builds in cranial vault and brain tissue presses down on the brain stem ○ Causes irreversible brain anoxia and death Diabetes Insipidus : decreased secretion of antidiuretic hormone ○ Excessive urine output, decreased urine osmolarity and hyperosmolarity 3L or more in 24 hours INTERVENTIONS ○ Administration of fluids ○ Electrolyte replacements ○ Admin synthetic vasopressin ( desmopressin ) SIADH: the result of increased secretions of ADH ○ Patient becomes volume overloaded and urine output diminishes ○ excessive thirst and hyponatremia, continuous secretion of vasopressin INTERVENTIONS: ○ Fluid restriction : less than 800 ml a day with no free water ○ Admin 3% hypertonic saline solution ○ Give bowel meds to decrease valsalva maneuver Nursing interventions: increased intracranial pressure Monitor respiratory status and lung sounds frequently Maintain patent airway Position HOB 0-60* to promote venous drainage, neutral position Avoid ○ hip flexion ○ valsalva maneuvers ( urinary retention, constipation, ascites ) these will cause intra abdominal pressure causing increased pressure in the brian ○ Coughing, sneezing, vomiting  Maintain a calm quiet environment Maintain fluid status : I+O Q1 hr in acute phase Use strict aseptic technique for management of ICP monitoring system Intrathoracic pressure : Alterations in intrathoracic pressure : coughing, sneezing, straining) abdominal distention, valsalva maneuvers Intracranial Surgery Craniotomy ○ Opening of the skull ○ Purposes: remove blood clot, relieve elevated ICP, remove tumor, control hemorrhages Craniectomy ○ Excision of portion of the skull Cranioplasty ○ Repair of cranial defect using a plastic or metal plate Burr holes ○ Circular openings for exploration or diagnosis, provide access to ventricles, shunting procedures, aspirate hematoma or abscess, or make a bone flap Preoperative care : medical management Pre Op diagnostic procedures Medications to reduce risk of seizures ○ Corticosteroids ○ Fluid restrictions ○ Hyperosmotic agents : Mannitol ( decreases water on the brain) ○ Diuretics may be used to reduce cerebral edema Antibiotics ( prophylactic ) Diazepam ( anxiety ) Preoperative nursing management Obtain baseline neurologic assessment Assess patient and family understanding Provide information, reassurance and support Postoperative care Detecting and reducing cerebral edema Relieving pain Preventing seizures Monitoring ICP and neurologic status Assessment of the patient undergoing intracranial surgery Frequent respiratory assessments ( including ABGs) Monitor vs and LOC frequently Note any potential signs of increased ICP Assess dressing for bleeding or CSF leak  Monitor for potential seizures, seizure precautions Monitor for complications Monitor fluid status and labs Possible complications intracranial surgery increased ICP Bleeding and hypovolemic shock Infection Fluid and electrolyte disturbances Csf leak Seizures Nursing interventions the patient undergoing intracranial surgery Maintain cerebral perfusion ○ Monitor respiratory status esp hypoxia or hypercapnia ○ Assess vs and neuro checks Q15mins-1hr Reduce cerebral edema ( peaks 24-36 hours) ○ Mannitol : pulls water from the brain ○ Dexamethasone “ helps keep permeable vessels from leaking IV Q6hr for 24-72 hours then po taper asap Control factors that increase ICP ○ Acetaminophen PRN for temps over 99.6 ○ Phenytoin, Levetiracetam PRN for potential seizures Avoid extreme head rotation ( head in neutral position ) ○ HOB may be flat or 30* according to needs related to the surgery Regulate temperature ○ Avoid extreme temps or sudden shifts in temp ○ Cover patient appropriately ○ Treat high temperature elevations vigorously ○ If patient starts shivering give meperidine Improving gas exchange ○ Turn and reposition every 2 hours ○ Encourage deep breathing and incentive spirometry ○ Suction and encourage coughing CAUTIOUSLY ( increases ICP) ○ Humidify oxygen to loosen secretions Manage sensory deprivation ○ Announce presence ○ Engage with patient Monitor I+O, weight, blood glucose, serum and urine electrolyte levels, osmolarity and specific gravity Prevent infections ○ Assess incision site for hematoma or infection ○ Assess patients for potential CSF leak ( clear fluid )  ○ Instruct patient to avoid coughing, sneezing, or nose blowing as this increases the risk for a CSF leak ○ Use strict aseptic technique Educate on self care Delirium Acute confusional state that starts with disorientation If untreated progresses to changes in LOC, irreversible brain damage, and possibly death Differentiate between delirium and dementia Confusion assessment method for screening Known risk factors: ○ Blood transfusions ○ Benzos ○ Older age ○ Concurrent dementia ○ Trauma Treatment : GOLD STANDARD Haloperidol Seizures Abnormal episodes of motor, sensory, autonomic, or psychic activity resulting from sudden, abnormal, uncontrolled electrical discharge form cerebral neurons Classifications of seizures ○ Focal: originates in one hemisphere ○ Generalized: occurs and engages bilaterally Convulsion ○ Specific seizure type of a motor seizure involving the entire body Generalized seizures Absence seizures: brief sudden lapses of consciousness Atonic seizures: sudden limpness in muscles Myoclonic seizures : brief jerking muscle movements Tonic seizures: sudden tension or stiffness may afflict the arms, legs or body Tonic clonic seizures/grand mal ; loss of consciousness and violent muscle contractions Status epilepticus Continual seizure that does not stop spontaneously Many types If untreated or not stopped can lead to death Emergency Plan of care patient with seizure Observation and documentation of patient signs and symptoms before during and after the seizure Patient safety and protection After seizure document, side lying, manage oral secretions  Seizure precautions : suction, low bed, 2-3 side rails up and padded Management seizures Prevention Medications start with one then add PRNs Surgery is intracranial tumor abscess cyst or vascular anomaly Headache AKA cephalalgia Primary headache ○ No known organic cause ○ Includes migrain, tension and cluster headache Secondary headache ○ Symptom with organic cause ie: brain tumor or aneurysm Headache assessment Detailed description of headache Med use and history Explicit signs and symptoms Neuro exam DX tests Thorough headache history Migraine Premonitory phase ○ Symptoms last hours to days before the migraine headache occurs ○ Symptoms: depression, irritability, feeling cold, food cravings, anorexia, change in activity level, increased urination, diarrhea or constipation ( prodrome symptoms may change with each migraine ) Aura phase ○ Focal neuro symptoms : visual disturbances, most common and may br hemianopic, numbness and tingling of the lips, face or hands, mild confusion, slight weakness of an extremity, drowsiness and dizziness Headache phase ○ Photophobia ○ Phonophobia ○ Allodynia ( sensitivity to touch) Post drome phase ○ Pain gradually subsides ○ Tiredness, weakness, and mood changes from hours to days ○ Neck and scalp muscle contractions ○ Physical excretion exacerbates pain ○ May sleep for extended periods Nursing management of headache : pain ○ Prophylactic meds  ○ Migraines and cluster headaches require abortive meds ○ Medications : triptans, ergotamine, NSAID, beta blockers ○ Provide comfort measures Quiet dark room Massage Local heat for tension Chapter 63 Head injury Broad classification that includes any injury to the head as result of trauma ○ Most common causes is TBI and falls Scalp wounds Tend to bleed heavily, and are portals for infection Signs and symptoms depend on severity and location Skull fractures Usually have localized, persistent pain Basilar fractures signs and symptoms ○ Fractures at the base of the skull ○ Bleeding from nose, pharynx, or ears ○ Battle sign - ecchymosis behind ears ○ CSF leak : halo sign - ring of fluid around the blood stain from drainage Pathophysiology of brain damage Primary injury : direct contact to head/brain during initial injury ○ EX: contusions, lacerations, external hematomas, concussion, skull fractures, subdural hematomas, diffuse axonal injury Secondary injury : damage evolving days after initial injury ○ Caused by cerebral edema, ischemia, or chemical changes associated from trauma Types of brain injuries Primary or direct injuries ○ Damage caused by an impact ○ Includes diffuse axonal injuries, the focal lesions of lacerations, contusion, hemorrhage Secondary injuries ○ Damage results from subsequent brain swelling, infection, and cerebral hypoxia ○ Includes concussion, infection, or hypoxic brain injury Types of traumatic brain injury Coup: direct impact injury, head is moving and object is stable ○ EX on roller blades and smack into a wall Counter coup: acceleration/deceleration injury the object is moving but the head is stable ○ EX car crash Shock wave : result of a bomb or shaken baby syndrome These brain injuries can cause herniation Types of brain injury Closed TBI: blunt trauma, acceleration/deceleration injury Open TBI: penetrating, object penetrates the brain or severe trauma that opens the scalp and skull Concussion: temporary loss of consciousness with no apparent structural damage Contusion: more severe injury with possible surface hemorrhage ○ Symptoms and recovery depend on the amount of damage and associated cerebral edema Diffuse axonal injury: widespread axon damage in the brain seen with head trauma ○ Patient develops immediate coma Intracranial bleeding : ○ Epidural hematoma ○ Subdural hematoma: acute, subacute, or chronic ○ Intracerebral hemorrhage and hematoma Focal and diffuse brain injuries Primary brain injuries contain two types ○ Focal ( contusion, laceration, hemorrhage) ○ Diffuse concussion, diffuse axonal Secondary injuries are often diffuse or multifocal, including edema, infection and hypoxic brain damage Concussion Occurs from a blow to the head Patient is admitted for observation or sent home Observation : report immediately if: ○ Changes in LOC ○ Difficulty awakening, lethargy, dizziness, confusion, irritability, anxiety ○ Difficulty in speaking or moving ○ Severe headache ○ Vomiting Patient should be aroused and assessed frequently Patient should have physical and cognitive rest for 1-2 days pending severity of concussion Total quiet for the brian Symptoms of a concussion Hazy, foggy, or groggy head feeling Headache or pressure in head Dizziness or balance issues Feeling confused or trouble remembering things Nausea and vomiting Post Concussion syndrome Concussion refers to an immediate and transient loss of consciousness accompanied by a brief period of amnesia after a blow to the head Recovery usually takes place in 24 hours Mild symptoms may persist for months  ○ Irritability ○ Headache ○ Insomnia ○ Poor concentration and memory Types of hematomas Epidural hematoma ○ Usually caused by head injury where the skull is fractured ○ Close to bone due to impact ○ An EMERGENCY situation ○ Blood collects in the space between the skull and dura ○ Brief loss of consciousness with return of lucid state ○ As hematoma expands increased ICP causes reduced LOC ○ Treatment: Reduce ICP Remove the clot Stop the bleeding Burr holes or craniotomy ○ Monitor and support vital body functions; respiratory support Subdural hematoma ○ Usually a tear in the small bridging veins that connect the veins on the surface of the cortex to dural sinuses ○ Develops in the area between the dura and the arachnoid ( subdural space ) ○ Blood between the dura and the brain Acute: symptoms develop in 24-48 hours Subacute : symptoms develop[e 48 hours to 2 weeks Treatment: requires immediate craniotomy and control of ICP Chronic : developed over weeks to months, causative injury may be minor or forgotten, clinical signs and symptoms may fluctuate Treatment : evacuation of clot ○ Reason it takes longer than epidural is because the blood has room to move and spread in the subdural area Traumatic intracerebral hematoma ○ May be single or multiple ○ Occur in any lobe of the brain but most common in the frontal and temporal lobes ○ Hemorrhage occurs into SUBSTANCE of the brain ○ Due to trauma or nontraumatic cause Treatment : Supportive care Control ICP Administer iV fluids slow ( 1ml/kg/hr), Electrolytes and antihypertensive medications Craniotomy or craniectomy to remove clot and control hemorrhage if possible Management head injury  Assess and diagnose extent of injury Assume cervical spine injury until rules out Apply cervical collar and maintain until cleared Preserve homeostasis and prevent 2* brain injury Supportive measures Respiratory support: intubation/mechanical ventilation Seizure precautions and prevention NG tube to reduce gastric motility and prevent aspiration Fluid and electrolyte maintenance Pain and anxiety management Nutrition Assessment TBI Health history that focuses on current injury, time and cause and the direction of the force of the blow Baseline assessment LOC- glasgow coma scale Frequent Q15 min and ongoing neuro assessment Multisystem assessment Nursing interventions TBI Ongoing assessment and monitoring are vital Maintain adequate airway Monitor neurologic function I+O and daily weights due to cerebral edema Monitor blood and urine Blood glucose Early initiation of NGT to promote adequate nutrition Strategies to prevent injury ○ Assess oxygenation ○ Assess bladder and urinary output ○ Assess for constriction caused by dressings and casts ○ Padded side rails ○ Mittens to avoid self injury, avoid restraints ○ Reduce environmental stimuli ○ Adequate lighting to reduce visual hallucinations ○ Minimize disruption of sleep wake cycles ○ Skin care, infection prevention Maintaining body temp ○ Maintain appropriate environmental temp ○ Use proper coverings ○ PRN acetaminophen for fever ○ Cooling blankets, cold baths, AVOID SHIVERING Spinal Cord injury Risk factors : young age, male gender, alcohol and drug use Major causes of death are pneumonia, pulmonary embolism, and sepsis Definition : damage to the neural elements of the spinal cord Causes: MVA, falls, violence, and sporting activities Pathophysiology spinal cord injury Results from concussion, contusion, laceration or compression of the spinal cord ( compression most likely a tumor) ○ Primary injury: the result of initial trauma and usually permanent ○ Secondary injury: resulting from SCI include edema and hemorrhage Treatment is needed to prevent partial injury from causing permanent damage Medications to decrease spinal pressure HIgh dose IV corticosteroids : methylprednisolone C Spine stabilization Skeletal traction ○ Traction is applied to the skeletal traction device through weights Halo device Spinal shock Sudden depression of reflex activity below the level of spinal injury Muscular flaccidity, lack of sensation and reflexes distal to the injury Neurogenic shock Loss of function of the ANS BP, HR and CO decrease Venous pooling occurs due to peripheral vasodilation Paralyzed portions of the body do not perspire Autonomic Dysreflexia *** ACUTE EMERGENCY*** Occurs after spinal shock has resolved and may occur years after injury Occurs in patient with SC lesions above T6 Autonomic nervous system responses are exaggerated Symptoms : ○ Severe pounding headache ○ Sudden increase in BP ○ Profuse diaphoresis ○ Nausea ○ Nasal congestion ○ Bradycardia Triggering stimuli : ○ Distended bladder ○ Constipation ○ Stimul;ation of the skin : belts, blankets, twisted johnny  ○ Distention or contraction of visceral organs Nursing interventions autonomic dysreflexia ○ Place in seated position to decrease blood pressure ○ Rapid assessment to identify and eliminate cause Empty the bladder Examine rectum for fecal mass Examine skin Examine for other stimuli ○ Admin ganglionic blocking agents : IV hydralazine hydrochloride ( Apresoline ) ○ Note risk for in patient with EHR Assessment spinal cord injury Monitor respirations and breathing patterns Lung sounds and cough\monitor for changes in sensory or motor function Assess for spinal shock Monitor for bladder retention or distention, gastric dilation, or ileus Temperature for potential hyperthermia Nursing interventions spinal cord injury Promoting effective breathing and airway clearance Improving mobility ○ PROM at least 4 times a day Strategies for compensating for sensory and perceptual alterations ○ Talking your patient through the steps of care Maintain skin integrity Catheterization NG tube to alleviate gastric distention High calorie, high protein, high fiber diets Bowel program with the use of stool softeners Traction pin care ○ Clean and assess underneath the traction devices ○ Pin site care : normal saline soaked cotton tip applicator gentle cleaning around the pin site Hygiene and skin care related to traction devices Assessment Tetraplegia and Paraplegia Head to toe Skin Bowel and bladder program Emotional and psychological responses Planning and goals for the patient with tetraplegia and paraplegia Attainment of some for of normality ** prevent spasticity, infection and sepsis Skin maintenance  Bladder management without infection Achievement of bowel control Achievement of sexual expression Strengthening coping mechanism Knowledge of long term management Absence of complications Chapter 64 Brain infections Meningitis Brain abscess Encephalitis Creutsfeldt-jakob disease Meningitis Inflammation of the meninges Types: bacterial and viral Transmitted through secretions ( most common ) or aerosol, most common in dense community Classified ○ Septic: bacteria ○ Aseptic: viral infections Symptoms ○ Headache ○ Fever ○ Altered LOC ○ Change in behavior ○ Nuchal rigidity ( neck with be stiff the patient will report that they can not look down or side to side ○ Positive kernig sign ○ Positive brudzinski sign ○ Photophobia ○ Nausea ○ Vomiting Kernig sign - Patient lying with thigh flexed on the abdomen the leg can not be completely extended Brudzinski sign - When the patient's neck is flexed it causes flexion of the hips and knees is produced Medical management of meningitis Prevention : meningococcal vaccine from 11-12 and booster at 16 Early admin of IV antibiotics  Dexamethasone : steroid to reduce swelling Treat for dehydration shock or seizures Nursing management of meningitis Frequent continuous assessment including VS and LOC Pain and fever management Protect patient from injury related to seizure or altered level of consciousness Monitor daily weight, serum electrolytes, urine volume, specific gravity, osmolarity Prevent complications associated with immobility : frequent turns Infection control precautions Measures to facilitate coping of the patient and family Encephalitis Infection of the brain or spinal cord parenchyma Manifested by Local necrotizing hemorrhage Progressive degeneration of nerve cell bodies Prominent edema Transmission : vector Can be viral ( HSV, West nile) , bacterial, or fungal Encephalitis slide 2 Acute inflammation of the brain tissue Most likely caused by viral infections like herpes simplex or viral infections contracted through mosquitos or fungal ] Symptoms ○ Headache ○ Fever ○ Confusion ○ Hallucinations ○ Vector borne - rash ○ Flaccid paralysis ○ Parkinson like movement Medical management ○ Acyclovir for HSV infection ○ Amphotercin for fungal infection Very strong antifungal administered iV has large risk of allergic reaction follow protocols give benadryl tylenol and decadron prior to first admin and monitor patient for any signs of anaphylaxis Nursing management ○ Frequent ongoing assessment ○ Supportive care ○ Monitoring ICP Brain abscess Collection of infectious material within the brain  Cause : bacteria most common Prevention : treat otitis media, rhinosinusitis Symptoms : ○ Headache usually worse in the morning ○ Fever ○ Vomiting ○ Neurologic deficits ○ Signs and symptoms of increased ICP Diagnosis by MRI or CT Medical management of brain abscess Control ICP Drain abscess Administer antibiotics and corticosteroids to decrease cerebral edema and treat infection Nursing management Frequent ongoing neuro assessment Admin medications Assess response to treatment Provide supportive care Creutsfeldt jakob disease Rare degenerative infectious transmissible spongiform encephalopathies Caused by prons Contracted through ingestion go infected beef Symptoms are impairment of ○ Affective ○ Sensory ○ Motor ○ Cognitive No treatment progressive and fatal Nursing management Prevention of disease transmission Multiple sclerosis A progressive immune-related demyelinating disease of the CNS Most common non traumatic cause of disability in young and middle aged adults Characterized by exacerbations and remissions over many years in several different sites of the CNS ○ As disease progressive there is less improvement between exacerbations and increasing neurologic dysfunction Typical symptoms ○ Fatigue ○ Weakness ○ Numbness  ○ Difficulty concentration ○ loss of balance ○ Pain ○ Visual disturbances During remission the myelin can regenerate and transmission of nerve impulses are restored Inflammation can recur causing exacerbations , can cause irreversible destruction of the myelin with dense scar tissue forming sclerotic plaques Assessment of patient with multiple sclerosis Neurologic defects Secondary complications : toileting, transfering, eating, hygiene, transfering Impact of disease on physical, social and emotional function and on lifestyle Patient and family coping Medical management Disease modifying therapies ○ Interferons ○ Glatirameter acetate ○ IV methylprednisolone Symptom management of muscle spasms ( baclofen), fatigue, ataxia, bowel and bladder control Nursing management Use collaborative approach Alternate activity and rest Bowel and bladder control Reinforce and encourage swallowing instructions ○ Possibly No straws, maybe thickened liquids Strategies to reduce aspiration ○ Eating meals in high fowlers, sips between bites Memory aides, structured environment Interventions to minimize stress Maintenance of temperature environment : avoid exposure to excess heats or excess cold Use assistive devices Support of coping Myasthenia gravis Autoimmune disease caused by antibody mediated loss of acetylcholine receptors in the neuromuscular junction Symptoms ○ Ptosis ○ Diplopia ○ Muscle weakness after use of the affected extremity ○ Hand grip may alternate between weak and normal ( milk maids grip) ○ Neck muscle may become weak ○ Weakness of facial muscles, swallowing and voice impairment  ○ Proximal limb weakness is common Medical management myasthenia gravis Directed at improving function and reducing/removing antibodies that destroy acetylcholine Meds ○ Anticholinesterase inhibitors : pyridostigmine bromide nor nostamine ○ Immunosuppressive therapies : corticosteroids prednisone or methylprednisolone Therapeutic plasma exchange Thymectomy Myasthenic crisis Result of disease exacerbation or precipitating event,most commonly a respiratory infection Severe generalized muscle weakness with respiratory or bulbar weakness ( cranial nerves 9-12) difficulty swallowing, weak tongue, weak facial muscles Patient may develop respiratory compromise or failure Cholinergic crisis Caused by overmedication with cholinesterase inhibitors Severe generalized muscle weakness with respiratory or bulbar weakness ( cranial nerves 9-12) difficulty swallowing, weak tongue, weak facial muscles Patient may develop respiratory compromise or failure Management Patient education in signs and symptoms of myasthenic crisis and cholinergic crisis Ensuring adequate ventilation ; intubation and mechanical ventilation may be needed Assessment and supportive measure ○ Maintain airway and respiratory support ○ Abgs serum electrolytes, I+O and daily weights ○ If patient can not swallow NG feedings may be required ○ Avoid sedatives and tranquilizers Guillain Barre syndrome Acute immune mediated polyneuropathy Acute , flu like illness usually precedes onset of symptoms Symptoms ○ Pain ○ Progressive ascending muscle weakness of limbs ○ Flaccid paralysis ○ Paresthesia and numbness ○ Can involve respiratory muscles ○ ANS involvement : postural hypotension, arrhythmia, facial flushing, abnormal sweating, urinary retention ○ Facial oculomotor or bulbar weakness ○ Ranges from mild weakness and spontaneous recovery to tetraplegia and ventilator support Medical management  Medical emergency Requires ICU Therapeutic plasma exchange and IVIG Recovery rates vary, but most patients recover completely Assessment guillain barre syndrome Ongoing assessment with emphasis on early detection of life threatening complications of respiratory failure, cardiac dysrhythmias, and DVT Monitor for changes in vital capacity and negative inspiratory force Assess VS frequently Patient and family coping NUrsing interventions Promote physical mobility and prevention of DVT ○ Support limbs in functional position ○ Passive ROM at least twice daily ○ Frequent position changes ○ Compression boots ○ Maintain adequate hydration Admin IV and parenteral nutrition as prescribed Carefully assess swallowing and gag reflex Develop a plan for communication Decreasing fear and anxiety Trigeminal neuralgia Condition of the fifth cranial nerve characterized by paroxysms of pain Most commonly occurs in the second and this branches of this nerve Vascular compression is the probable cause Occurs more often with women in the fifth and sixth decades of life Pain can occur with stimulation such as washing face, brushing teeth, eating or draft in air Patients may avoid eating, neglect hygiene, and even isolate themselves to prevent attack Medical management Anticonvulsants : carbamazepine Gabapentin and baclofen Phenytoin adjunctive therapy Surgical treatment ○ Microvascular decompression of the trigeminal nerve ○ Radiofrequency thermal regulation ○ Percutaneous balloon microcompression Nursing interventions Patient education related to pain prevention and treatment regimens Measures to reduce and prevent pain Measures to maintain hygiene, washing face at peak of pain meds  Strategies to promote nutrition : soft food, chew on unaffected side, avoid hot and cold food Interventions to address anxiety depression and insomnia Bell's palsy Facial paralysis caused by the 7th cranial nerve caused by unilateral inflammation Symptoms ○ Unilateral facial muscle weakness or paralysis ○ Facial distortion ○ Increased lacrimation ○ Painful sensations in the face ○ May have difficulty with speech or eating Most patients recover in 3-5 weeks and disorder rarely recurs Medical Corticosteroid therapy and pain medication NURSING Reinforce education that stroke has not occured Protection from eye injury Facial exercises and massage to maintain muscle tone