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UTA NURS 4581 Exam 3

UTA NURS 4581 Critical Care Exam 3

intracranial pressure the hydrostatic force measured in the brain cerebrospinal fluid compartment
Factors that influence ICP under normal circumstances changes in (1) arterial pressure, (2) venous pressure, (3) intraabdominal and intrathoracic pressure, (4) posture, (5) temperature (fever), and (6) blood gases, particularly CO2 levels.
ICP normal range 5 to 15 mm Hg
ventriculostomy “Gold standard” for monitoring ICP; a specialized catheter is inserted into the lateral ventricle and coupled to an external transducer. Measures pressure within ventricles, facilitates removal/sampling of CSF, intraventricular drug administration.
Cerebral blood flow (CBF) the amount of blood in milliliters passing through 100 g of brain tissue in 1 minute
CBF normal range global: 50 mL/min; white matter: 25 mL/min; gray matter: 75 mL/min
cerebral perfusion pressure (CPP) the pressure needed to ensure blood flow to the brain.
Calculation of Cerebral Perfusion Pressure (CPP) MAP-ICP
CPP normal range 60 to 100 mm Hg
Calculation of MAP [SBP + 2(DBP)] / 3
MAP where autoregulation is effective 50 to 150 mm Hg
Decreased MAP manifestations CBF decreases, and symptoms of cerebral ischemia, such as syncope and blurred vision, occur.
Increased MAP manifestations the vessels are maximally constricted, and further vasoconstrictor response is lost.
stage 1 ICP there is high compliance. The brain is in total compensation, with accommodation and autoregulation intact. An increase in volume (in brain tissue, blood, or CSF) does not increase the ICP.
stage 2 ICP the compliance is beginning to lessen, and an increase in volume places the patient at risk of increased ICP.
stage 3 ICP significant reduction in compliance. Any small addition of volume causes a great increase in ICP. Compensatory mechanisms fail, loss of autoregulation, and the patient will exhibit manifestations of increased ICP
stage 4 ICP ICP rises to lethal levels with little increase in volume. Herniation occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a one of lesser pressure. If herniation continues to occur, brainstem death is imminent.
Factors affecting cerebral blood flow Carbon dioxide, oxygen, and hydrogen ion concentration
Vasogenic cerebral edema most common cerebral edema; mostly in white matter; changes to endothelial lining allow leakage of macromolecules from the capillaries into the surrounding extracellular space, resulting in flow of fluid from the intravascular to the extravascular space.
Cytotoxic cerebral edema occurs most often in the gray matter; develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia, sodium depletion, and syndrome of inappropriate antidiuretic hormone (SIADH) secretion.
Interstitial cerebral edema the result of rupture of the CSF brain barrier and is usually a result of obstructive or uncontrolled hydrocephalus.
Increased ICP manifestation change in LOC, change in VS (Cushing’s triad), ocular signs, decreased motor function (Decorticate and decerebrate posturing), headache, vomiting
Cushing’s triad neurologic emergency; systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations
Decorticate posturing Flexion of arms, wrists, and fingers with adduction in upper extremities. Extension, internal rotation, and plantar flexion in lower extremities.
Decerebrate posturing All four extremities in rigid extension, with hyperpronation of forearms and plantar flexion of feet.
Ventriculostomy zeroing reference point the tragus of the ear
Stroke affecting anterior cerebral artery feeds the medial and anterior portions of the frontal lobes, affecting higher-order processes (e.g., judgment, reasoning)
middle cerebral artery feeds the outer portions of the frontal, parietal, and superior temporal lobes
posterior cerebral artery feeds the medial portions of the occipital and inferior temporal lobes
Stroke nonmodifiable risk factors age (doubles each decade after 55 years of age, 2/3 occur >65 yrs of age), gender (more common in men, more deaths in women), ethnicity/race (African Americans have higher incidence), family history/heredity.
Conditions that increase risk of stroke HTN, diabetes, migraines, inflammatory conditions, sickle cell disease
transient ischemic attack (TIA) transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of the brain; clinical symptoms typically last less than 1 hour
transient ischemic attack (TIA) manifestations If the carotid system is involved, temporary loss of vision in one eye (amaurosis fugax), a transient hemiparesis, numbness or loss of sensation, or a sudden inability to speak.
ischemic stroke includes thrombotic and embolic strokes; stroke that results from inadequate blood flow to the brain due to partial or complete occlusion of an artery
penumbra a border zone of reduced blood flow around the core area of ischemia where ischemia is potentially reversible.
Thrombotic stroke most common cause of stroke; The process of clot formation (thrombosis) results in a narrowing of the lumen, which blocks the passage of the blood through the artery.
lacunar stroke type of thrombotic stroke; a stroke resulting from occlusion of a small penetrating artery with development of a cavity in the place of the infarcted brain tissue
lacunar stroke manifestations pure motor hemiplegia, pure sensory stroke (contralateral loss of all sensory modalities), contralateral leg and face weakness with arm and leg ataxia, and isolated motor or sensory stroke.
Thrombotic stroke manifestations Most do NOT have a decreased LOC in the first 24 hours. Ischemic stroke symptoms may progress in the first 72 hours as infarction and cerebral edema increase.
Embolic stroke second most common cause of stroke; An embolus is a blood clot or other debris circulating in the blood. When it reaches and artery in the brain that is too narrow to pass through, it lodges there and blocks the flow of blood.
Embolic stroke manifestations rapid occurrence of severe clinical symptoms; usually remains conscious, although he or she may have a headache
Hemorrhagic stroke includes intracerebral and subarachnoid strokes; a burst blood vessel may allow blood to seep into and damage brain tissues until clotting shuts off the leak.
intracerebral hemorrhage accounts for 10% of all strokes; a type of hemorrhagic stroke in which bleeding within the brain is caused by a rupture of a blood vessel; prognosis is poor (30-day mortality rate is 40-80%)
intracerebral hemorrhage manifestations neurologic deficits, headache, nausea, vomiting, decreased level of consciousness (in about 50% of patients), and hypertension.
subarachnoid hemorrhage a stroke resulting from intracranial bleeding into the cerebrospinal fluid–filled space between the arachnoid and pia mater membranes on the surface of the brain
subarachnoid hemorrhage manifestations Sudden onset of a severe headache that is different from a previous headache and typically the “worst headache of one's life”, focal neurologic deficits (including cranial nerve deficits), nausea, vomiting, seizures, and stiff neck
aneurysm congenital or acquired weakness of the arterial wall resulting in dilation and ballooning of the vessel
right-brain damage manifestations paralyzed left side (hemiplegia); left-sided neglect; spatial-perceptual deficits; tends to deny or minimize problems; rapid performance, short attention span; impulsive, safety problems; impaired judgment
left-brain damage manifestations paralyzed right side (hemiplegia); impaired speech/language aphasias; impaired right/left discrimination; slow performance, cautious; aware of deficits (depression, anxiety); impaired comprehension r/t language and math
aphasia an abnormal neurologic condition in which language function is disordered or absent because of an injury to certain areas of the cerebral cortex
dysphasia difficulty related to the comprehension or use of language
dysarthria a disturbance in the muscular control of speech resulting from interference in the control and execution over the muscles of speech
Homonymous hemianopsia common problem after a stroke; blindness in the same half of each visual field which causes unilateral neglect and inability to judge distances
Stroke preventative therapy control HTN, DM; treatment of underlying cardiac problem; no smoking; limit alcohol intake; drug therapy (platelet inhibitors [e.g., aspirin] and anticoagulation therapy); surgical therapy
Antiplatelet drugs used to prevent stroke Aspirin (most common), ticlopidine (Ticlid), clopidogrel (Plavix), dipyridamole (Persantine), and combined dipyridamole and aspirin (Aggrenox)
ticlopidine (Ticlid) Antiplatelet drugs used to prevent stroke
clopidogrel (Plavix) Antiplatelet drugs used to prevent stroke
dipyridamole (Persantine) Antiplatelet drugs used to prevent stroke
combined dipyridamole and aspirin (Aggrenox) Antiplatelet drugs used to prevent stroke
treatment of choice for individuals with atrial fibrillation who have had a TIA Oral anticoagulation using warfarin
surgical therapy to prevent stroke Carotid endarterectomy, Stenting of carotid artery, Transluminal angioplasty, Extracranial-intracranial bypass, Surgical interventions for aneurysms at risk of bleeding
Stroke acute care management Maintain airway, Fluid therapy (NS), pulse ox monitoring, adequate oxygenation & BP, remove clothing, CT scan (w/o contrast), position head midline and elevate 30 degrees, administer thrombolytics (for ischemic stroke), NPO until swallow reflex evaluated
Ischemic Stroke management Tissue plasminogen activator (tPA) IV or intraarterial and MERCI retriever.
Tissue plasminogen activator (tPA) use and guidelines administered IV within 3-4.5 hrs of onset of signs of ischemic stroke to reestablish blood flow through a blocked artery to prevent cell death
Tissue plasminogen activator (tPA) screening noncontrast CT or MRI scan to rule out hemorrhagic stroke, blood tests for coagulation disorders, and screening for recent history of gastrointestinal bleeding, stroke, or head trauma within the past 3 months, or major surgery within 14 days.
MERCI retriever Removes blood clots in patients experiencing ischemic strokes. Wire pushed through end of a catheter up to carotid artery reshapes itself into tiny loops that latch onto the clot and pull it out. To prevent the clot from breaking off, a balloon inflates.
Hemorrhagic Stroke management Surgical decompression if indicated; Clipping or coiling of aneurysm; nimodipine (Nimotop) administration to decrease vasospasm; Antiseizure drugs, such as phenytoin (Dilantin) or levetiracetam (Keppra), are given if a seizure occurs.
nimodipine (Nimotop) use to treat cerebral vasospasm either before or following aneurysm clipping or coiling; given to patients with subarachnoid hemorrhage to decrease the effects of vasospasm and minimize cerebral damage
nimodipine (Nimotop) drug alert Assess blood pressure and apical pulses before administration. If pulse is ≤60 beats/min or systolic BP is <90 mm Hg, hold medication and contact physician.
phenytoin (Dilantin) use antiseizure medication
levetiracetam (Keppra) use antiseizure medication
The LICOX brain tissue oxygen system a catheter inserted through an intracranial bolt. The system measures oxygen in the brain (PbtO2), brain tissue temperature, and intracranial pressure (ICP)
Anterior cerebral stroke manifestations Motor and/or sensory deficit (contralateral), sucking or rooting reflex, rigidity, and gait problems, loss of proprioception, fine touch
Middle cerebral stroke manifestations Dominant side: aphasia, motor and sensory deficit, hemianopsia; Nondominant side: neglect, motor and sensory deficit, hemianopsia
Posterior cerebral stroke manifestations Hemianopsia, visual hallucination, spontaneous pain, motor deficit
Vertebral stroke manifestations Cranial nerve deficits, diplopia, dizziness, nausea, vomiting, dysarthria, dysphagia, and/or coma
AGNOSIA Disturbance in interpretation of visual, tactile, or auditory information. Loss of ability to recognize objects.
ANOSOGNSIA Real or pretended ignorance of the presence of disease.
EXPRESSIVE (MOTOR) APHASIA Difficulty communicating through spoken word, gestures or writing.
RECEPTIVE (SENSORY) APHASIA Difficulty comprehending written (visual) or spoken (auditory) words.
APRAXIA Inability to use body part for specific motor tasks although the part is not paralyzed.
DYSPHAGIA Difficulty swallowing due to muscular weakness.
EMBOLUS Mass of undissolved material carried in flow of blood frequently causing occlusion of a vessel.
ENDARTERECTOMY Surgical removal of atherosclerotic tissue from the innermost lining of an artery. To prevent stroke, this procedure may be performed on the carotid artery (or arteries).
HEMIANESTHESIA Partial or complete loss of sensation involving one half of the body.
HEMIANOPSIA Disturbance/loss of vision in one half of the visual field.
HEMIPARESIS Slight paralysis of one side of the body.
HEMIPLEGIA Paralysis of one half of the body.
HYPOVIGILANCE Ann affective state in which there is decreased alertness and decreased attentiveness.
PARESIS Incomplete paralysis.
PARESTHESIA Tingling, pin-prick sensation due to disorder of sensory nervous system.
PROPIOCEPTION Sense of the position of a joint in space.
PTOSIS Dropping or drooping of an organ or part, as the upper eyelid from paralysis.
SUBLUXATION A partial or incomplete dislocation.
THROMBUS Blood clot formed within a blood vessel or the heart.
Receptive (Comprehending) Aphasia communication techniques allow time to understand, keep commands short and simple, speak slowly, keep to personal and familiar subjects, use visual cues (gestures, writing), stay in view while speaking, one person speak at a time, keep conversation at their level
Expressive (Communicating) Aphasia communication techniques make patient want to speak, permit mistakes, give time to speak with no interruptions, listen attentively, don’t force to speak or see people, don’t compare current to past speech and don’t ridicule
“ATES” of ICP management ElevATE, StrAIGHT, RegulATE, SeparATE, IntubATE, CoagulATE, MedicATE, HyperventilATE, EvacuATE, OperATE
Myasthenia gravis (MG) an autoimmune disease of the neuromuscular junction characterized by the fluctuating weakness of certain skeletal muscle groups
Myasthenia gravis (MG) muscles most often involved those used for moving the eyes and eyelids, chewing, swallowing, speaking, and breathing
Myasthenia gravis (MG) cause an autoimmune process in which antibodies attack acetylcholine (ACh) receptors, resulting in a decreased number of ACh receptor (AChR) sites at the neuromuscular junction, preventing ACh molecules from attaching and stimulating muscle contraction
Myasthenic crisis an acute exacerbation of myasthenia gravis triggered by infection, surgery, emotional distress, or overdose or inadequate medication
Cholinergic crisis Overdose of anticholinesterase drugs resulting in increased ACh at the receptor sites, remission (spontaneous or after thymectomy)
Myasthenic crisis v. Cholinergic crisis If myasthenic crisis, patient will show improved strength after IV administration of anticholinesterase drugs (Tensilon test)
Tensilon test in a patient with MG reveals improved muscle contractility after IV injection of the anticholinesterase agent edrophonium chloride (Tensilon)
Myasthenia gravis (MG) management Drug therapy, surgery (thymectomy), plasmapheresis
Drug therapy for Myasthenia gravis (MG) anticholinesterase drugs, alternate-day corticosteroids, and immunosuppressants
Pyridostigmine (Mestinon) use the most successful anticholinesterase inhibitor in long-term treatment of Myasthenia gravis (MG)
amyotrophic lateral sclerosis (ALS) aka Lou Gehrig’s disease; a rare progressive neurologic disorder characterized by loss of motor neurons and by weakness and atrophy of the muscles of the hands, forearms, and legs, spreading to involve most of the body and face
ALS manifestations weakness of the upper extremities (usually, but may begin in legs), dysarthria, and dysphagia
ALS management no cure, death usually occurs 2-6 yrs from diagnosis; Riluzole (Rilutek) used to slow progression
Riluzole (Rilutek) use slows the progression of ALS; works to decrease the amount of glutamate (an excitatory neurotransmitter) in the brain.
Guillain-Barré syndrome an acute, rapidly progressing, and potentially fatal form of polyneuritis believed to be caused by a cell-mediated immunologic reaction directed at the peripheral nerves
Guillain-Barré syndrome manifestations mild to severe and develops within 1-3 weeks after upper respiratory or GI infection; Weakness of the lower extremities (evolving more or less symmetrically with distal muscles more affected), parasthesia, paralysis, hypotonia, areflexia, sensory loss
Guillain-Barré syndrome management supportive care, particularly ventilatory support; plasmapheresis or IV immunoglobulin (Sandoglobulin) within first 2 weeks of onset
Plasmapheresis used to treat autoimmune diseases (e.g., myasthenia gravis and Guillain-Barré syndrome); the removal of plasma containing components causing or thought to cause disease and replacement by substitute fluids such as saline, fresh-frozen plasma, or albumin
Most common cause of head injury MVAs and Falls
Factors that predict a poor outcome after head injury the presence of an intracranial hematoma, older age of the patient, abnormal motor responses, impaired or absent eye movements or pupillary light reflexes, early sustained hypotension, hypoxemia or hypercapnia, and ICP levels greater than 20 mm Hg.
Glasgow Coma Scale assessment tool for altered states of consciousness that evaluates motor responses, verbal responses, and eye opening
GCS indicating a 30% to 70% chance of survival below 8
Timing of death after head injury immediately, within 2 hrs, or within 3 weeks
major complications associated with scalp laceration blood loss and infection
Linear skull fracture Break in continuity of bone without alteration of relationship of parts caused by low-velocity injuries
basilar skull fracture a specialized type of linear fracture that occurs when the fracture involves the base of the skull
basilar skull fracture manifestations otorrhea (CSF leakage from the ear), bulging of tympanic membrane, Battle's sign, periorbital ecchymosis (raccoon eyes), tinnitus or hearing difficulty, rhinorrhea (CSF leakage from the nose), facial paralysis, conjugate deviation of gaze, vertigo
Tests to determine if fluid leaking from nose or ear is CSF if no blood, glucose test (Dextrostix, Tes-Tape strip)—positive if CSF; if blood is present, look for halo/ring sign (when dripped on white pad/towel, yellowish ring encircles blood if CSF is present)
Depressed skull fracture Inward indentation of skull caused by a powerful blow
Simple skull fracture Linear or depressed skull fracture without fragmentation or communicating lacerations caused by low to moderate impact
Comminuted skull fracture Multiple linear fractures with fragmentation of bone into many pieces caused by direct, high-momentum impact
Compound skull fracture Depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity caused by severe head injury
Frontal skull fracture manifestations Exposure of brain to contaminants through frontal air sinus, possible association with air in forehead tissue, CSF rhinorrhea, or pneumocranium
Orbital skull fracture manifestations Periorbital ecchymosis (raccoon eyes), optic nerve injury
Temporal skull fracture manifestations Boggy temporal muscle because of extravasation of blood, oval-shaped bruise behind ear in mastoid region (Battle's sign), CSF otorrhea, middle meningeal artery disruption, epidural hematoma
Parietal skull fracture manifestations Deafness, CSF or brain otorrhea, bulging of tympanic membrane caused by blood or CSF, facial paralysis, loss of taste, Battle's sign
Posterior fossa skull fracture manifestations Occipital bruising resulting in cortical blindness, visual field defects; rare appearance of ataxia or other cerebellar signs
Concussion a sudden transient mechanical head injury, such as a blow or explosion, with disruption of neural activity and a change in the level of consciousness (usually brief, < 5 min)
Postconcussion syndrome manifestations develops 2 weeks to 2 months after injury; persistent headache, lethargy, personality and behavioral changes, shortened attention span, decreased short-term memory, and changes in intellectual ability
Diffuse axonal injury (DAI) usually develops in 12 to 24 hours after injury; widespread axonal damage occurring after a mild, moderate, or severe traumatic brain injury (TBI)
Diffuse axonal injury (DAI) manifestations decreased LOC (> 5 min), increased ICP, decortication or decerebration, and global cerebral edema; 90% of patients with DAI remain in a persistent vegetative state
Contusion the bruising of the brain tissue within a focal area without altering the integrity of the pia mater and arachnoid layers; may contain areas of hemorrhage, infarction, necrosis, and edema, and frequently occurs at a fracture site
coup-contrecoup injury brain moves inside the skull due to high-energy or high-impact injury mechanisms causing contusions or lacerations both at the site of the direct impact of the brain on the skull (coup) and at a secondary area of damage on the opposite side (contrecoup)
brain lacerations actual tearing of the brain tissue; often occur in association with depressed and open fractures and penetrating injuries
brain laceration management surgical repair impossible and prognosis is pour; antibiotics until meningitis is ruled out, and preventing secondary injury related to increased ICP
epidural hematoma neurologic emergency usually associated with a linear fracture crossing a major artery in the dura, causing a tear; collection of blood between the dura and the inner surface of the skull, producing compression of the dura matter and thus of the brain
epidural hematoma manifestations initial period of unconsciousness at the scene, with a brief lucid interval (up to 12 hours) followed by a decrease in LOC; pupil dilation on same side; decorticate or decerebrate posturing; headache, nausea and vomiting, or focal findings
epidural hematoma management Rapid surgical intervention to evacuate the hematoma and prevent cerebral herniation, along with medical management for increasing ICP
subdural hematoma collection of blood between the dura mater and the arachnoid layer of the meninges of the brain that is usually of venous origin, usually caused by injury
acute subdural hematoma manifestations manifests within 24 to 48 hours of the injury; HA, drowsiness, agitation, confusion, deterioration in LOC, fixed and ipsilateral pupil dilation, contralateral hemiparesis or profound coma
subacute subdural hematoma manifestations usually occurs within 2 to 14 days of the injury; similar to acute (; HA, drowsiness, agitation, confusion, deterioration in LOC, fixed and ipsilateral pupil dilation, contralateral hemiparesis or profound coma) except appear more slowly.
chronic subdural hematoma manifestations develops over weeks or months after a seemingly minor head injury
chronic subdural hematoma commonly affected populations older adults and alcoholics due to cerebral atrophy and increased incidence of falls
subdural hematoma management craniectomy, craniotomy (acute), evacuation and decompression (all types), membranectomy (chronic), burr holes
intracerebral hematoma collection of blood within the parenchyma of the brain possibly from the rupture of an intracerebral vessel at the time of a head injury
intracerebral hematoma manifestations patient suddenly deteriorates 6-10 days after trauma
intracerebral hematoma management surgery with significant ICP problems
Poor 6-month recovery of head injury associated with lower GCS score, abnormal pupillary reflex on admission, lower systolic BP, older age
Blunt trauma body strikes or is struck by an object
Penetrating trauma an open injury in which a foreign body impales or passes through the body tissues
Level I Trauma Center a comprehensive regional resource that is a tertiary care facility central to the trauma system capable of providing total care for every aspect of injury – from prevention through rehabilitation.
Level II Trauma Center able to initiate definitive care for all injured patients.
Level III Trauma Center demonstrated ability to provide prompt assessment, resuscitation, surgery, intensive care and stabilization of injured patients and emergency operations.
Level IV Trauma Center demonstrated ability to provide advanced trauma life support (ATLS) prior to transfer of patients to a higher level trauma center; provides evaluation, stabilization, and diagnostic capabilities for injured patients.
Triage system categorizes patients so most critical are treated first; (category 1: sickest/unstable to category 5: stable, minor illness or injury)
Trauma ABC… A: Airway with c-spine; B: Breathing; C: Circulation; D: Disability (neuro exam); E: Expose control; F: full VS, focused adjuncts, family; G: give comfort measures (pain control); H: History/Head-to-toe assessment; I: inspect posterior surfaces
Emergency assessment primary survey focuses on airway, breathing, circulation, disability, and exposure/environmental control. It serves to identify life-threatening conditions so that appropriate interventions can be initiated.
Jaw-thrust maneuver recommended procedure for opening the airway of an unconscious patient with a possible neck or spinal injury
AVPU A: alert, V: responsive to voice, P: responsive to pain, and U: unresponsive
Emergency assessment secondary survey begins after initiating lifesaving interventions identified during primary survey; a brief, systematic process that aims to identify all injuries
MIVT mnemonic for assessing history of injury; M: mechanism of injury; I: injury suspected; V: Vital Signs; T: Treatment in field
AMPLE mnemonic for assessing patient’s health history; A: allergies; M: Medication; P: Past health history; L: last meal; E: events/environment leading to illness/injury
Chest trauma and thoracic injuries fractured ribs; flail chest; ruptured diaphragm; contusions; pneumothorax; hemothorax
Most common type of chest injury from blunt trauma fractured ribs
Fractured ribs manifestations pain at the site of injury, especially during inspiration and coughing; splinting the affected area and taking shallow breaths to try to decrease the pain; atelectasis and pneumonia may develop because of decreased ventilation and retained secretions.
Fractured rib management DON’T strap or bind chest; NSAID, opioids, and nerve blocks are used to reduce pain and aid with deep breathing and coughing. Patient teaching should emphasize deep breathing, coughing, use of incentive spirometry, and use of pain medications.
flail chest instability of the chest wall resulting from multiple rib fractures
flail chest manifestations Paradoxic movement of chest wall, respiratory distress, may be associated hemothorax, pneumothorax, pulmonary contusion
flail chest management O2 as needed to maintain O2 saturation; analgesia; stabilize flail segment with positive pressure ventilation (CPAP, BiPAP), or intubation and mechanical ventilation; treat associated injuries
pneumothorax a collection of air or gas in the pleural space causing the lung to collapse
management of chest wound with object that caused it still in place do not remove it until a physician is present. Stabilize the impaled object with a bulky dressing.
pneumothorax manifestations Dyspnea, decreased movement of involved chest wall, diminished or absent breath sounds on the affected side, hyperresonance to percussion
pneumothorax management Chest tube insertion with flutter valve or chest drainage system
tension pneumothorax rapid accumulation of air in the pleural space causing severely high intrapleural pressures with resultant tension on the heart and great vessels and decreased cardiac output
tension pneumothorax manifestations Cyanosis, air hunger, violent agitation, tracheal deviation away from affected side, subcutaneous emphysema, neck vein distention, hyperresonance to percussion
tension pneumothorax management Medical emergency: needle decompression followed by chest tube insertion with chest drainage system
hemothorax accumulation of blood in the pleural space
hemothorax manifestations Dyspnea, diminished or absent breath sounds, dullness to percussion, decreased hemoglobin, shock depending on blood volume lost
hemothorax management Chest tube insertion with chest drainage system; autotransfusion of collected blood, treatment of hypovolemia as necessary
cardiac tamponade compression of the heart produced by fluid accumulation in the pericardial sac
cardiac tamponade manifestations Muffled, distant heart sounds, hypotension, neck vein distention, increased central venous pressure
cardiac tamponade management Medical emergency: pericardiocentesis with surgical repair as appropriate
abdominal trauma manifestations guarding of abdominal wall (peritonitis); hard, distended abdomen (intraabdominal bleeding); decreased/absent bowel sounds; contusions/abrasions/bruising on abdomen; abdominal pain; pain over scapula; hematemesis/hematuria; & signs of hypovolemic shock
Cullen’s sign Ecchymosis around the umbilicus which may indicate retroperitoneal hemorrhage
Grey Turner’s sign Ecchymosis around the flanks which may indicate retroperitoneal hemorrhage
Kehr’s sign pain over the scapula caused by irritation of the phrenic nerve by free blood in the abdomen or ruptured spleen
Abdominal girth increase with abdominal bleed 1 inch/500 mL - 1 L of blood
Increased amylase etiology Injuries to pancreas
Peritoneal lavage most sensitive technique for detecting injuries to hollow organs; large catheter inserted into abdomen, attempt to aspirate, if < 10 mL aspirated, inject saline and drain, observe fluid for gross abnormalities, especially blood, & send to lab
Bowel sounds in the chest indicates may indicate a diaphragmatic rupture
cause of premature death in the patient with tetraplegia (paralysis of both arms and legs) usually related to compromised respiratory function
tetraplegia paralysis of the arms, legs, and trunk occurring with spinal cord damage at C8 or above
paraplegia paralysis characterized by motor and/or sensory loss in the lower limbs and trunk
primary spinal cord injury initial mechanical disruption of axons as a result of stretch or laceration
secondary spinal cord injury ongoing, progressive damage that occurs after the initial injury
cause of permanent damage from spinal cord injuries Edema extends above and below the injury and compresses the spinal cord, thus increasing the ischemic damage
spinal shock temporary, immediate failure of all spinal cord function at the time of injury below the level of cord damage resulting in flaccid paralysis, loss of reflexes, and loss of sympathetic innervation
spinal shock resolution signs return of reflexes (especially flexors to noxious cutaneous stimuli), a state of hyperreflexia rather than flaccidity, and reflex emptying of the bladder.
neurogenic shock neurologic syndrome caused by the loss of vasomotor tone caused by spinal cord injury at the fifth thoracic (T5) vertebra or above and characterized by hypotension, bradycardia, and warm, dry extremities
Flexion injury of the cervical spine manifestations ruptures the posterior ligaments.
Hyperextension injury of the cervical spine manifestations ruptures the anterior ligaments.
Compression fractures of the cervical spine manifestations crush the vertebrae and force bony fragments into the spinal canal.
Flexion-rotation injury of the cervical spine manifestations most unstable injury that most often implicated in severe neurologic deficits; often results in tearing of ligamentous structures that normally stabilize the spine.
Skeletal level of injury the vertebral level where there is the most damage to vertebral bones and ligaments
Neurologic level of injury the lowest segment of the spinal cord with normal sensory and motor function on both sides of the body.
Most common level of spinal cord injury Cervical and lumbar injuries are most common because these levels are associated with the greatest flexibility and movement
Level of lesion that causes tetraplegia cervical (C8 and above)
Level of lesion that causes paraplegia thoracic and lumbar (T1 and below)
Complete cord involvement results in total loss of sensory and motor function below the level of the lesion (injury).
Incomplete cord involvement results in a mixed loss of voluntary motor activity and sensation and leaves some tracts intact.
central cord syndrome damage to the central spinal cord characterized by microscopic hemorrhage, edema of the central spinal cord, and compression on anterior horn cells
central cord syndrome manifestations Motor weakness and sensory loss are present in both the upper and lower extremities, but the upper extremities are affected more than the lower ones.
Anterior cord syndrome caused by damage to the anterior spinal artery. This results in compromised blood flow to the anterior spinal cord.
Anterior cord syndrome manifestations motor paralysis and loss of pain and temperature sensation below the level of injury. Because the posterior cord tracts are not injured, sensations of touch, position, vibration, and motion remain intact.
Brown-Séquard syndrome damage to one half of the spinal cord characterized by spastic paralysis on the body's injured side, loss of postural sense (proprioception), and loss of the senses of pain and heat on the other side of the body
Brown-Séquard syndrome manifestations loss of motor function and position and vibratory sense, as well as vasomotor paralysis on the same side (ipsilateral) as the lesion. The opposite (contralateral) side has loss of pain and temperature sensation below the level of the lesion.
Posterior cord syndrome compression or damage to the posterior spinal artery. It is a very rare condition.
Posterior cord syndrome manifestations loss of proprioception with pain, temperature sensation, and motor function below the level of the lesion remaining intact.
conus medullaris syndrome and cauda equina syndrome result from damage to the very lowest portion of the spinal cord (conus) and the lumbar and sacral nerve roots (cauda equina)
conus medullaris syndrome and cauda equina syndrome manifestations flaccid paralysis of the lower limbs and areflexic (flaccid) bladder and bowel.
American Spinal Injury Association (ASIA) Impairment Scale commonly used for classifying the severity of impairment resulting from spinal cord injury; uses assessments of motor and sensory function to determine neurologic level and completeness of injury
Spinal cord injury level that corresponds with total loss of respiratory muscle function above the level of C4
Respiratory complications r/t spinal cord injuries total loss of function (above C4), respiratory insufficiency, hypoventilation, ineffective cough (d/t paralysis of abdominal and intercostal muscles), neurogenic pulmonary edema (d/t increased SNS activity and fluid overload)
Respiratory management r/t spinal cord injuries if loss of respiratory muscle function, mechanical ventilation
Cardiovascular complications r/t spinal cord injuries Bradycardia (above T6), hypotension, hypovolemia,
Cardiovascular management r/t spinal cord injuries In marked bradycardia (heart rate <40 beats/min), appropriate drugs (atropine) to increase the heart rate and prevent hypoxemia are necessary. IV fluids or vasopressor drugs may be required to support blood pressure.
Urinary system complications r/t spinal cord injuries retention, reflex emptying
Urinary system management r/t spinal cord injuries initial Foley catheter, then intermittent catheterization
GI system complications r/t spinal cord injuries hypomotility (if above T5) causing paralytic ileus and gastric distention; stress ulcers; intraabdominal bleeding; neurogenic bowel (areflexic bowel with decreased sphincter tone, then reflexes return and tone is enhanced)
Signs of GI bleed Continued hypotension in spite of vigorous treatment and decreased hemoglobin and hematocrit; expanding girth of abdomen
GI system management r/t spinal cord injuries NG/OG tube for intermittent suctioning, Metoclopramide (Reglan) for delayed gastric emptying; H2-receptor blockers, (Zantac, Pepcid), and proton pump inhibitors (Protonix IV, Prilosec, Prevacid) to prevent the occurrence of ulcers; regular bowel program
Metoclopramide (Reglan) use to treat delayed gastric emptying
Integumentary system complications r/t spinal cord injuries skin breakdown over bony prominences
Poikilothermism the adjustment of the body temperature to the room temperature
Thermoregulation complications r/t spinal cord injuries Poikilothermism (adjustment of the body temperature to the room temperature); decreased ability to sweat or shiver
Metabolic complications r/t spinal cord injuries metabolic alkalosis (from NG suctioning) or acidosis (d/t decreased tissue perfusion); electrolyte imbalances (from NG suctioning); weight loss
Peripheral Vascular complications DVT (PE leading cause of death in spinal cord injury patients)
Criteria for surgery in spinal cord injuries (1) evidence of cord compression, (2) progressive neurologic deficit, (3) compound fracture of the vertebrae, (4) bony fragments (may dislodge and penetrate the cord), and (5) penetrating wounds of the spinal cord or surrounding structures.
Medication given within 8 hours of spinal cord injury that significantly improves motor function and sensation methylprednisolone (MP)
methylprednisolone (MP) contraindications penetrating trauma to the spinal cord and should be used with caution in the elderly population
Autonomic dysreflexia (also known as autonomic hyperreflexia) life-threatening; a massive uncompensated cardiovascular reaction mediated by the sympathetic nervous system. It occurs in response to visceral stimulation once spinal shock is resolved in patients with spinal cord lesions.
Autonomic dysreflexia most common precipitating cause a distended bladder or rectum
Autonomic dysreflexia manifestations HTN (up to 300 systolic), throbbing HA, marked diaphoresis above lesion, bradycardia (30-40), piloerection (erection of body hair), flushing of the skin above lesion, blurred vision or spots in the visual fields, nasal congestion, anxiety, & nausea.
Autonomic dysreflexia prevention Straight catheterization should be done every 4 to 6 hours, and Foley catheters should be checked frequently to prevent kinks in the tubing; maintain bowel regularity.
Marked perspiration above the level of injury concern Autonomic dysreflexia
Autonomic dysreflexia management elevation of the head of the bed 45 degrees or sitting the patient upright, notify physician, and assess to determine the cause. Possible immediate catheterization or checking of existing catheter for kinks, or digital rectal exam (after anesthetic).
mass casualty incident a human-caused (e.g., biologic warfare) or natural (e.g., hurricane) event or disaster that overwhelms a community's ability to respond with existing resources
BE NICE biologics, explosives, nuclear, chemical spills, environmental
Green MCI triage minor (e.g., sprain)
Yellow MIC triage non-life threatening (e.g., open fracture)
Red MIC triage life threatening (e.g., shock)
Blue MIC triage non-salvageable
Black MIC triage dead
Thermal burns burns caused by flame, flash, scald, or contact with hot objects and are the most common type of burn injury
Chemical burns tissue injury and destruction from acids, alkalis, and organic compounds.
Alkali vs. Acid burn management Alkali burns can be more difficult to manage than acid burns since alkaline substances are not neutralized by tissue fluids as readily as acid substances. Alkalis adhere to tissue, causing protein hydrolysis and liquefaction.
Smoke and inhalation injuries result from the inhalation of hot air or noxious chemicals and can cause damage to the tissues of the respiratory tract.
accounts for the majority of deaths at a fire scene Carbon monoxide (CO) poisoning
inhalation injury above the glottis (upper airway injury) thermally produced and may be caused by the inhalation of hot air, steam, or smoke.
Clues that Inhalation injury above the glottis (upper airway injury) is likely presence of facial burns, singed nasal hair, hoarseness, painful swallowing, darkened oral and nasal membranes, carbonaceous sputum, history of being burned in an enclosed space, and clothing burns around the chest and neck.
inhalation injury below the glottis (lower airway injury) usually chemically produced. Tissue damage is related to the duration of exposure to smoke or toxic fumes.
inhalation injury below the glottis (lower airway injury) manifestations pulmonary edema or acute respiratory distress syndrome (ARDS); may not appear until 12 to 24 hours after the burn
Electrical burns the result of intense heat generated from an electric current.
Risks of electrical injuries dysrhythmias or cardiac arrest, severe metabolic acidosis, and myoglobinuria, which can lead to acute tubular necrosis (ATN).
Burn Severity determined by (1) depth of burn, (2) extent of burn calculated in percent of total body surface area (TBSA), (3) location of burn, and (4) patient risk factors.
partial-thickness burn varying degrees of epidermal and dermal skin injury in which some skin elements remain viable for regeneration
full-thickness burn destruction of all skin elements and subcutaneous tissues with possible involvement of muscles, tendons, and bones
face, neck and circumferential burns to chest/back complications inhibited respiratory function and possible inhalation injury and respiratory mucosal damage.
Hands, feet, joints, and eye burns complications self-care difficulty; challenging to manage because of superficial vascular and nerve supply systems and the need to maintain their function during healing.
Ear, nose, buttocks, and perineum burn complication susceptible to infection
Circumferential burn to extremities complications circulatory compromise distal to the burn with subsequent neurologic impairment of the affected extremity; compartment syndrome.
Risk factors for poor prognosis for recovery from burns older adults; preexisting cardiovascular, respiratory, or renal disease; DM or peripheral vascular disease; General physical debilitation from any chronic disease; concurrently sustained fractures, head injuries, or other trauma
Rule of nines Guide for determining total body surface area affected or the extent of a burn; 9% for each side of each leg; 9% for both arms for each side; 18% for trunk for each side; 4.5% for head for each side; and 1% for groin
greatest initial threat to a patient with a major burn hypovolemic shock
burn shock patho burn > increased vascular permeability > 1) edema—decreased blood volume AND 2) decreased intravascular volume—Increased Hct—increased viscosity > increased peripheral resistance > burn shock
Burn complications dysrhythmias, hypovolemic shock, ischemia, paresthesias, necrosis, & eventually gangrene
Parkland Formula of Fluid Resuscitation (>20% TBSAB) 4 mL LR x kg x %TBSAB; give ½ in first 8 hours, remaining over next 16 hours
Multiples of Maintenance (<20% TBSAB) 10-15% TBSAB use 1 ½ x maintenance; 15-20% TBSAB use 2 x maintenance
Adequate fluid resuscitation urine output 0.5 to 1 mL/kg/hr; 75 to 100 mL/hr for electrical burn patient with evidence of hemoglobinuria/myoglobinuria
Adequate fluid resuscitation cardiac factors Mean arterial pressure (MAP) greater than 65 mm Hg, systolic BP greater than 90 mm Hg, heart rate less than 120 beats per minute.
Debridement removal of dirt, foreign objects, damaged tissue, and cellular debris from a wound or a burn to prevent infection and promote healing
cultured epithelial autograft skin grafts grown from biopsy specimens obtained from the patient's own skin
hematopoietic stem cell transplant transplantation of peripheral stem cells
brain death a clinical diagnosis of an irreversible loss of all brain functions, including the brainstem
Criteria for brain death coma or unresponsiveness, absence of brainstem reflexes, and apnea
Graft-versus-host disease (GVHD) occurs when an immunoincompetent (immunodeficient) patient is transfused or transplanted with immunocompetent cells.
Cold ischemic time time and organ is outside of the body when being transported from the deceased doneor to the recipient
Kidney cold ischemic time can be preserved for up to 72 hours, but most transplant surgeons prefer to transplant kidneys before the cold ischemic time reaches 24 hours.
Liver cold ischemic time 20 hrs
Pancreas cold ischemic time 12 hrs
Hearts cold ischemic time 4-6 hrs
Organ recipient criteria <70 years, absence of infection, absence of general malignancy
Organ recipient contraindications serious active infection or sepsis; severe disease in other organs; recent or disseminated cancer; current substance abuse; severe cachexia (underweight); active peptic ulcer disease; psychiatric disorders; repeated noncompliance
human leukocyte antigen (HLA) system The antigens responsible for rejection of genetically unlike tissues
panel of reactive antibodies (PRA) indicates the recipient's sensitivity to various HLAs before receiving a transplant
standard triple therapy for immunosuppression for transplants usually includes a calcineurin inhibitor, a corticosteroid, and mycophenolate mofetil (CellCept).
Drugs that prevent a cell-mediated (Helper T cell) attack against the transplanted organ Calcineurin inhibitors (e.g., tacrolimus and cyclosporine)
Drugs used pre-treatment that bind with the CD3 antigen found on the surface of human thymocytes and mature T cells Monoclonal antibodies (e.g., Muromonab-CD3 [Orthoclone OKT3], daclizumab [Zenapax] and basiliximab [Simulect])
Monoclonal antibody side effects flu-like: fever, rigors, headache, myalgias, and various GI disturbances.
Drugs used as induction therapy to severely immunosuppress an individual immediately after transplantation Polyclonal antibodies (e.g., Lymphocyte immune globulin [Atgam])
Cardiac transplantation indications End-stage HF; Severe decompensated inoperable valvular heart disease; Recurrent life-threatening dysrhythmias; Any cardiac abnormalities that severely limit normal function and/or have a mortality risk of greater than 50% at 2 yr
Cardiac transplantation contraindications Chronologic age > 70 or physiologic age > 65; Life-threatening illness (e.g., malignancy); Advanced cerebral or peripheral vascular disease; Active infection; Severe pulmonary disease requiring ventilator after transplant
Test used to detect rejection of transplanted heart and timing of tests an endomyocardial biopsy (EMB) is obtained on a weekly basis for the first month, monthly for the following 6 months, and yearly thereafter.
Heart’s Breath Test measures methylate alkalies in patient’s breath and compares with results of endo to separate less severe (low levels) to more severe (higher levels)
Kidney transplant complications Rejection of transplant (Hyperacute, Acute, Chronic); Susceptibility to infection; Cardiovascular disease; Malignancies; Recurrence of renal disease; Corticosteroid-related complications
Leading cause of death after renal transplant cardiovascular disease
Lung transplant complications infections, acute rejection, bronchiolitis obliterans
Leading cause of death in the early period after lung transplantation bacterial, viral, fungal, or protozoal infections
Indications for Liver transplantation viral hepatitis (leading indication); congenital biliary abnormalities (biliary atresia), inborn errors of metabolism, hepatic malignancy (confined to the liver), sclerosing cholangitis, fulminant hepatic failure, and chronic end-stage liver disease
Liver transplant complications bleeding, rejection, and infection
allogeneic transplantation stem cells are acquired from a donor who, through human leukocyte antigen (HLA) tissue typing, has been determined to be HLA matched to the recipient.
Syngeneic transplantation a type of allogeneic transplant that involves obtaining stem cells from one identical twin and infusing them into the other.
autologous transplantation patients receive their own stem cells back following myeloablative (destroying bone marrow) chemotherapy
Stem cell transplant complications Bacterial, viral, and fungal infections; graft-versus-host disease; veno-occlusive disease; bleeding; renal insufficiency; GI issues
Graft Rejection of organs occurs as a normal immune response to foreign tissue; controlled by immunosuppression therapy, ABO and HLA matching, and ensuring that the crossmatch is negative
Hyperacute (antibody-mediated, humoral) rejection occurs minutes to hours after transplantation because the blood vessels are rapidly destroyed because the person had preexisting antibodies against the transplanted tissue or organ.
Acute rejection most commonly manifests in the first 6 months after transplantation; usually mediated by the recipient's lymphocytes, which have been activated against the donated (foreign) tissue or organ
Chronic rejection a process that occurs over months or years and is irreversible. Chronic rejection can occur for unknown reasons or from repeated episodes of acute rejection.
crossmatch uses serum from the recipient mixed with donor lymphocytes to test for any preformed anti-HLA antibodies to the potential donor organ; positive crossmatch is a contraindication to transplantation
Cirrhosis chronic progressive disease of the liver characterized by extensive degeneration and destruction of the liver parenchymal cells
hepatic encephalopathy changes in neurologic and mental function resulting from high levels of ammonia in the blood that a damaged liver cannot detoxify
Asterixis flapping tremor (liver flap) commonly affecting the arms and hands that is a manifestation of hepatic encephalopathy
Fetor hepaticus musty, sweet odor of the patient's breath which occurs in some patients with encephalopathy from the accumulation of digestive by-products that the liver is unable to degrade.
esophageal varices distended, tortuous, fragile veins at the lower end of the esophagus that result from portal hypertension
caput medusae ring of varices around the umbilicus
cirrhosis metabolic manifestations hypokalemia; hyponatremia; hypoalbuminemia
cirrhosis early manifestations GI disturbances: anorexia, dyspepsia, flatulence, nausea and vomiting, and change in bowel habits (diarrhea or constipation); RUQ or epigastric pain; fever, lassitude, slight weight loss, and enlargement of the liver and spleen.
Cirrhosis late manifestations result from liver failure and portal HTN. Jaundice, peripheral edema, and ascites; skin lesions, hematologic disorders, endocrine disturbances, and peripheral neuropathies. In the advanced stages the liver becomes small and nodular.
Factors involved in the development of ascites portal hypertension; increased flow of hepatic lymph; decreased serum colloidal oncotic pressure; hyperaldosteronism; impaired water excretion
Cirrhosis management I&Os, daily weights, abdominal girth and extremity measurements to assess extent of edema; paracentesis (to remove excess fluid from abdominal cavity); monitor for hemorrhage and low blood count; avoid heavy lifting or stress; assess for LOC; drug therapy
Cirrhosis drug therapy no specific drug therapy for cirrhosis. However, a number of drugs are used to treat symptoms and complications of advanced liver disease.
Drug therapy for Hemostasis and control of bleeding in esophageal varices, constriction of splanchnic arterial bed vasopressin (Pitressin); octreotide (Sandostatin)
Cirrhosis diet high calorie (3000 cal/day) with high carbohydrate and moderate to low levels of fat. Low sodium (with ascites and edema); monitor potassium; fluid restriction (< 1 L/day)
Sengstaken-Blakemore Tube Type of tube used for balloon tamponade in patients with esophageal and/or gastric varices; the gastric and esophageal balloons put mechanical compression on the varices.
Total portal diversion used with patients with portal hypertension used to control flow of the blood in the varices
Transjugular intrahepatic portosystemic shunt (TIPS) a nonsurgical procedure in which a tract (shunt) between the systemic and portal venous systems is created to redirect portal blood flow
Positioning for dyspnea due to ascites A semi-Fowler's or Fowler's position allows for maximal respiratory efficiency
acute pancreatitis an acute inflammatory process of the pancreas caused by autodigestion and marked by symptoms of acute abdomen and escape of pancreatic enzymes into the pancreatic tissues
Trypsin autodigestive pancreatic enzyme that causes edema, necrosis, and hemorrhage
Elastase autodigestive pancreatic enzyme that causes hemorrhage
Phospholipase A autodigestive pancreatic enzyme that causes fat necrosis
Lipase autodigestive pancreatic enzyme that causes fat necrosis
Kallikrein autodigestive pancreatic enzyme that causes edema, vascular permeability, smooth muscle contraction, and shock
Most common causes of pancreatitis alcoholism (men), biliary tract disease (women); trauma, infection, drugs
Edematous pancreatitis mild pancreatitis or interstitial pancreatitis
Necrotizing pancreatitis severe pancreatitis
Pancreatitis manifestation sudden onset, deep, piercing, continuous/steady LUQ or midepigastric pain that commonly radiates to the back. nausea and vomiting, low-grade fever, leukocytosis, hypotension, tachycardia, and jaundice.
Pancreatitis complications pseudocyst, which may perforate, causing peritonitis, or rupture into the stomach or duodenum
Pseudocyst potentially life threatening complication of pancreatitis; a cavity continuous with or surrounding the outside of the pancreas filled with necrotic products and liquid secretions, such as plasma, pancreatic enzymes, and inflammatory exudates
Pseudocyst manifestations abdominal pain, palpable epigastric mass, nausea, vomiting, and anorexia
Lab tests for acute pancreatitis elevated serum amylase and lipase. Other findings include an increase in liver enzymes, triglycerides, glucose, and bilirubin and a decrease in calcium.
Pancreatitis management (1) relief of pain; (2) prevention or alleviation of shock; (3) reduction of pancreatic secretions; (4) correction of fluid and electrolyte imbalances; (5) prevention or treatment of infections; and (6) removal of the precipitating cause, if possible
First priority in managing acute pancreatitis administration of IV fluids and electrolyte repletion
Most effective means of relieving pain from pancreatitis NPO status
bariatric surgery a surgical procedure that is used to treat morbid obesity
bariatric surgery criteria guidelines BMI ≥40 or a BMI ≥35 with one or more severe obesity-related medical complications (e.g., hypertension, type 2 diabetes mellitus, heart failure, or sleep apnea) AND documentation of three unsuccessful attempts at medically supervised weight loss programs
Restrictive bariatric surgeries reduces the size of the stomach, which causes the patient to feel full quicker
Benefits of restrictive bariatric surgery vs. malabsorptive Since digestion is not altered, the risk of anemia or cobalamin deficiency is low. Procedures can be performed using a laparoscopic approach, decreasing postoperative pain, hospital stays, and the rate of wound infection and hernia formation
Malabsorptive bariatric surgeries bypass various lengths of the small intestine so that less food is absorbed
Vertical banded gastroplasty (VBG) aka stomach stapling; involves partitioning the stomach into a small pouch (15-30 mL capacity) in the upper portion along the lesser curvature of the stomach.
Complications of vertical banded gastroplasty (VBG) dehiscence of the stomach staple line or frequent, prolonged vomiting
adjustable gastric banding (AGB) aka Lap-Band or Realize Band; most common restrictive procedure and preferred option for patients who are surgical risks; the stomach size is limited by an inflatable band placed laparoscopically around the fundus of the stomach
vertical sleeve gastrectomy about 85% of the stomach is removed leaving a sleeve- shaped stomach
Biliopancreatic diversion (BPD) removal of approximately three fourths of the stomach to produce both restriction of food intake and reduction of acid output
Biliopancreatic Diversion with Duodenal Switch variation of the BPD procedure involves a duodenal switch where surgeons leave a larger portion of the stomach intact and a small part of the duodenum, keeping the pyloric valve, which helps prevent dumping syndrome
Biliopancreatic diversion (BPD) complications increased risk of gallstone formation; intestinal irritation and ulcers; abdominal bloating and foul-smelling stool or gas; very liquid and frequent stools; malnutrition and anemia
Roux-en-Y gastric bypass (RYGB) procedure a combination of restrictive and malabsorptive surgery; he stomach size is decreased with a gastric pouch anastomosis that empties directly into the jejunum
Most common bariatric procedure performed in the United States Roux-en-Y gastric bypass (RYGB) procedure
Roux-en-Y gastric bypass (RYGB) procedure complications dumping syndrome
Dumping syndrome gastric contents empty too rapidly into the small intestine, overwhelming its ability to digest nutrients
Nutritional therapy post-gastrectomy dumping syndrome divide meals into 6 small feedings; fluids not taken with meals (at least 30-45 min before/after); avoid concentrated sweets; increase protein and fats (meat, cheese, and eggs); cobalamin injection monthly
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