NURS 6550 Acute Care Study Guide for Midterm Walden University.docx

NURS 6550 Acute Care Study Guide for Midterm Walden U NURS 6550 Acute Care Study Guide for Midterm • Evaluate patients with psychosocial health conditions • Develop differential diagnoses for patients with psychosocial health conditions • Develop treatment plans for patients with psychosocial health conditions Generalized anxiety disorder diagnosis criteria- Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 months, about a number of events or activities (such as work or school performance).  B. The person finds it difficult to control the worry.  C. The anxiety and worry are associated with three (or more) of the following six symptoms (with at least some symptoms present for more days than not for the past 6 months). Note: Only one item is required in children.  (1) restlessness or feeling keyed up or on edge 
(2) being easily fatigued 
(3) difficulty concentrating or mind going blank 
(4) irritability 
(5) muscle tension 
(6) sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep) Primary neurotransmitter in PTSD- Due to the traumatic stress of PTSD victims, the neurotransmitters that fuel the sympathetic versus parasympathetic system get out of balance. As a Yale University journal review states, “It has been suggested that alterations in NE [norepinephrine], E [epinephrine], and 5-HT [5HTP] may have relevance for symptoms commonly seen in survivors with PTSD * PTSD diagnosis and treatment-assessing history of exposure to a perceived or actual life threatening event, serious injury or sexual violence, symptoms lasting more than 1 month. Disturbance causes clinically significant distress or impairment in functioning H) The disturbance is not attributable to the physiological effects of a substance or other medical condition DSM-5 recognizes a “with dissociative symptom” specifier when the PTSD symptoms are accompanied by persistent or recurrent depersonalization or derealization. The specifier “with delayed expression” should be included if the full criteria for PTSD are not met for more than 6 months following the trauma.  The traumatic event is persistently re-experienced: • Nightmares • Intrusive thoughts of the traumatic event • Flashbacks • Marked emotional distress when exposed to traumatic reminders • Strong physiologic reaction when exposed to traumatic reminders Treatment psychotherapy (cognitive processing, prolonged exposure therapy, eye-movement desensitizing) . SSRIs (sertraline, paroxetine) clonidine 0.1mg at bed time, prazosin 2-10mg for nightmare, antiseizure meds for anger management (carbamazepine 400-800mg daily), clonazepam 1-4mg daily for anxiety, Trazodone 25-100mg for sleep. Treatment of acute panic attacks- What are the medications for initial/first line therapy- SL 0.5-1 mg alprazolam, clonazepam 0.5-1mg, antidepressants, SSRIs (sertraline 25mg/day for 1 week, then 50mg) Inpatient treatment of depression- ECT o What are the therapies for patient’s that won’t eat, take meds, etc. When is serotonin norepinephrine reuptake inhibitor indicated, when is it contraindicated? For pain neuropathy/fibromyalgia Venlafaxine dosing, when is follow up? What are you monitoring? - Blood pressure monitoring, arrhythmias DOSE is 150-225 mg daily. Patients should be cautioned about the concomitant use of Venlafaxine tabletsand NSAIDs, aspirin, warfarin, or other drugs that affect coagulation since combined use of psychotropic drugs that interfere with serotonin reuptake and these agents has been associated with an increased risk of bleeding (see PRECAUTIONS,Abnormal Bleeding). Usual Adult Dose for Anxiety Extended release:
Initial dose: 75 mg orally once a day
Maintenance dose: May increase in daily increments of 75 mg orally at intervals of no less than 4 days
Maximum dose: 225 mg orally per day Usual Adult Dose for Panic Disorder Extended release:
Initial dose: 37.5 mg orally once a day
Maintenance dose: May increase dose in daily increments of 75 mg orally at intervals of no less than 7 days
Maximum dose: 225 mg orally per day Usual Adult Dose for Depression Immediate release:
Initial dose: 37.5 mg orally twice a day or 25 mg orally 3 times a day
Maintenance dose: May increase in daily increments of up to 75 mg orally at intervals of no less than 4 days
Maximum dose: (moderately depressed outpatients): 225 mg orally per day
Maximum dose (severely depressed inpatients): 375 mg orally per day
Comments:
-Daily dosage may be divided in 2 or 3 doses/day Endogenous depression pathophysiology is best described as? Endogenous depression. Endogenous depression (melancholia) is an atypical sub-class of the mood disorder, major depressive disorder (clinical depression). Endogenous depression occurs due to the presence of an internal (cognitive, biological) stressor instead of an external (social, environmental) stressor. No apparent outside cause. Exogenous is caused by something (stress, some event) Differences between panic attacks and panic disorder? Panic attacks are recurrent, unpredicted episodes of intense surges of anxiety accompanied by marked physical manifestations. Panic Disorder Someone with generalized anxiety disorder (GAD) has chronic anxiety, and a tendency to become over-anxious about issues which would not normally cause concern. Panic disorder is characterized by repeated episodes of panic attacks, in which the individual is overcome by feelings of fear and dread. What are Major Depressive disorder symptoms?- physical & cognitive symptoms, loss of interest and pleasure(anhedonia) withdrawal from activities and guilt, poor concentration, worthlessness, fatigue Identify the primary neurotransmitter in PTSD • PTSD diagnosis and treatment, meds (families/common meds)? Familiarize yourself with the side effects of Lithium- GI, tremors-treat with propranolol 20-60mg a day, weakness, somnolence, polyuria (reduced renal response ADH) , polydipsia (increased plasma renin concentration), thyroid, EKG changes, long term effects cogwheel rigidity, affect Common adverse effects of atypical antipsychotics- anticholinergic side effects dry mouth which can cause increases caloric liquid intake (wt gain & hyponatremia) blurred vision, urinary retention, delayed gastric emptying, esophageal reflux, ileus, delirium, acute glaucoma, sexual disturbances, and orthostatic hypotension, EKG changes prolonged QT Mental status changes in elderly… how do you evaluate? Mental status changes related to UTI in elderly Assessment of Delirium in geriatric patients- Acute onset, fluctuating course, deficits in attention not memory. Elders with dementia and driving – there is no gold standard assessment, consider the severity of the dementia ( severe should not drive), consider comorbidities and medications, ability to do IADLS, , may need to be assessed by a driver rehab specialist. Short Confusion Assessment Method (Short CAM): what things are assessed? Acute onset and fluctuating course, inattention and either disorganized thinking or ALOC. Types of dementia, know differences? Alzheimer's disease- Alzheimer's disease Most common type of dementia; accounts for an estimated 60 to 80 percent of cases. Symptoms: Difficulty remembering recent conversations, names or events is often an early clinical symptom; apathy and depression are also often early symptoms. Later symptoms include impaired communication, poor judgment, disorientation, confusion, behavior changes and difficulty speaking, swallowing and walking. Revised guidelines for diagnosing Alzheimer’s were published in 2011 recommending that Alzheimer’s be considered a slowly progressive brain disease that begins well before symptoms emerge. Brain changes: Hallmark abnormalities are deposits of the protein fragment beta-amyloid (plaques) and twisted strands of the protein tau (tangles) as well as evidence of nerve cell damage and death in the brain Vascular dementia- Vascular dementia Previously known as multi-infarct or post-stroke dementia, vascular dementia is less common as a sole cause of dementia than Alzheimer’s, accounting for about 10 percent of dementia cases. Symptoms: Impaired judgment or ability to make decisions, plan or organize is more likely to be the initial symptom, as opposed to the memory loss often associated with the initial symptoms of Alzheimer's. Occurs from blood vessel blockage or damage leading to infarcts (strokes) or bleeding in the brain. The location, number and size of the brain injury determines how the individual's thinking and physical functioning are affected. Brain changes: Brain imaging can often detect blood vessel problems implicated in vascular dementia. In the past, evidence for vascular dementia was used to exclude a diagnosis of Alzheimer's disease (and vice versa). That practice is no longer considered consistent with pathologic evidence, which shows that the brain changes of several types of dementia can be present simultaneously. When any two or more types of dementia are present at the same time, the individual is considered to have mixed dementia Dementia with Lewy bodies (DLB)- Dementia with Lewy bodies (DLB) back to top Symptoms: People with dementia with Lewy bodies often have memory loss and thinking problems common in Alzheimer's, but are more likely than people with Alzheimer's to have initial or early symptoms such as sleep disturbances, well-formed visual hallucinations, and slowness, gait imbalance or other parkinsonian movement features. Brain changes: Lewy bodies are abnormal aggregations (or clumps) of the protein alpha-synuclein. When they develop in a part of the brain called the cortex, dementia can result. Alpha-synuclein also aggregates in the brains of people with Parkinson's disease, but the aggregates may appear in a pattern that is different from dementia with Lewy bodies. The brain changes of dementia with Lewy bodies alone can cause dementia, or they can be present at the same time as the brain changes of Alzheimer's disease and/or vascular dementia, with each abnormality contributing to the development of dementia. When this happens, the individual is said to have mixed dementia. Mixed dementia- Mixed dementia In mixed dementia abnormalities linked to more than one cause of dementia occur simultaneously in the brain. Recent studies suggest that mixed dementia is more common than previously thought. Brain changes: Characterized by the hallmark abnormalities of more than one cause of dementia —most commonly, Alzheimer's and vascular dementia, but also other types, such as dementia with Lewy bodies. Parkinson's disease- Parkinson's disease As Parkinson's disease progresses, it often results in a progressive dementia similar to dementia with Lewy bodies or Alzheimer's. Symptoms: Problems with movement are common symptoms of the disease. If dementia develops, symptoms are often similar to dementia with Lewy bodies. Brain changes: Alpha-synuclein clumps are likely to begin in an area deep in the brain called the substantia nigra. These clumps are thought to cause degeneration of the nerve cells that produce dopamine. Frontotemporal dementia- Frontotemporal dementia Includes dementias such as behavioral variant FTD (bvFTD), primary progressive aphasia, Pick's disease, corticobasal degeneration and progressive supranuclear palsy. Symptoms: Typical symptoms include changes in personality and behavior and difficulty with language. Nerve cells in the front and side regions of the brain are especially affected. Brain changes: No distinguishing microscopic abnormality is linked to all cases. People with FTD generally develop symptoms at a younger age (at about age 60) and survive for fewer years than those with Alzheimer's. Creutzfeldt-Jakob disease- CJD is the most common human form of a group of rare, fatal brain disorders affecting people and certain other mammals. Variant CJD (“mad cow disease”) occurs in cattle, and has been transmitted to people under certain circumstances. Symptoms: Rapidly fatal disorder that impairs memory and coordination and causes behavior changes. Brain changes: Results from misfolded prion protein that causes a "domino effect" in which prion protein throughout the brain misfolds and thus malfunctions. Normal pressure hydrocephalus-Normal pressure hydrocephalus Symptoms: Symptoms include difficulty walking, memory loss and inability to control urination. Brain changes: Caused by the buildup of fluid in the brain. Can sometimes be corrected with surgical installation of a shunt in the brain to drain excess fluid. Huntington's Disease back to top Huntington’s disease is a progressive brain disorder caused by a single defective gene on chromosome 4. Symptoms: Include abnormal involuntary movements, a severe decline in thinking and reasoning skills, and irritability, depression and other mood changes. Brain changes: The gene defect causes abnormalities in a brain protein that, over time, lead to worsening symptoms Wernicke-Korsakoff Syndromeback to top Korsakoff syndrome is a chronic memory disorder caused by severe deficiency of thiamine (vitamin B-1). The most common cause is alcohol misuse. Symptoms: Memory problems may be strikingly severe while other thinking and social skills seem relatively unaffected. Brain changes: Thiamine helps brain cells produce energy from sugar. When thiamine levels fall too low, brain cells cannot generate enough energy to function properly Aricept and dosing and patient teaching? Donepezil 5 mg PO once daily max dose 10mg daily, side effects diarrhea, nausea, anorexia, wt loss, syncopal. D/C med if no benefits or having side effects, or financial burdens, evaluate after 2 months of highest dose Most important fact about this drug To maintain any improvement, Aricept must be taken regularly. If the drug is stopped, its benefits will soon be lost. Patience is in order when starting the drug. It can take up to 3 weeks for any positive effects to appear. How should you take this medication? Aricept should be taken once a day just before bedtime. Be sure it's taken every day. If Aricept is not taken regularly, it won't work. It can be taken with or without food. If you miss a dose... Make it up as soon as you remember. If it is almost time for the next dose, skip the one that was missed and go back to the regular schedule. Never double the dose. Management of disinhibition in elderly- • Physical findings when death is imminent- dyspnea, nausea/vomiting. Pain, constipation, fatigue, delirium/agitation, Coolness. Hands, arms, feet, and legs may be increasingly cool to the touch. ...Confusion. ... Sleeping. ... Incontinence. ... Restlessness. ... Congestion. ... Urine decrease. ... Fluid and food decrease, Little appetite and thirst. Fewer and smaller bowel movements and less pee, More pain, Changes in blood pressure, breathing, and heart rate. Limits of pain medication on dying patient- use long acting opioids around the clock and short acting opioids for breakthrough pain , do not undertreat pain in the dying pt (in rare cases palliative sedation may be needed, use of versed or phenobarbital IV with monitoring) Theories about successful aging…familiarize yourself with them- A person was deemed to have successfully aged if the person (1) lived free of disability or disease; (2) had high cognitive and physical abilities; and (3) was interacting with others in meaningful ways Reducing risk factors for disease/disability • Genetic risks decline with age; lifestyle factors determine risk • Risk factors can be reduced/modified (e.g. weight loss program effect on cardiovascular disease) • Increased within-person variability is predictor of mortality (better than just their mean level of performance) • Maximizing cognitive and physical function • Predictors of cognitive function: education, strenuous activity around home, peak pulmonary flow rate, self-efficacy • Education: due to direct beneficial effect or leads to life-long learning? • Cognitive function can be enhanced; plasticity persists in older age • Continuing engagement with life • Social relations: Being part of social network determines longevity, esp for men • Socio-emotional (affection) vs instrumental (direct assistance) support • Productive activity predictors: functional capacity, education, and self-efficacy • Response to stress • More ‘stressful life events’ and ‘daily hassles’; need resilience to recover and meet criteria for successful aging • Activity theory • Continuity theory • Disengagement theory Activity Theory The activity theory occurs when individuals engage in a full day of activities and maintain a level of productivity to age successfully. The activity theory basically says: the more you do, the better you will age. It makes a certain kind of sense, too. People who remain active and engaged tend to be happier, healthier, and more in touch with what is going on around them. Same goes for people of any age. Often, the activity theory is dismissed to some degree because it falls a little flat. It isn't sufficient to just be busy, like the definition states. You can't wake up every day and do the same thing, like riding a stationary bike, and expect to age well. This theory was taken and used by many program designers for the elderly, who filled older folks' schedules with busy work and required them to complete tasks. A heightened level of activity is needed, but it needs to be engaging and fulfilling, rather than just busy work. The theory also fails to consider maintenance of one's mid-life or changes that are made when entering retired or older life. If I was a high-powered, high-stress executive and I retire and go into pottery making, am I going to age successfully? Not likely, particularly if I enjoyed my job as an executive. Maybe what is needed is another theory that looks at the lifespan instead of just older age. Continuity Theory The continuity theory states that individuals who age successfully continue habits, preferences, lifestyle, and relationships through midlife and later. Again, this theory makes a certain kind of intuitive sense. People who are doing well in midlife, who are happy, healthy, and just plain dandy should carry over the habits and ideals that made them that way. Basically, good stuff should be continued because it's good stuff! An easy way of thinking about how the continuity theory can demonstrate successful aging is by considering your own life. The disengagement theory of aging states that "aging is an inevitable, mutual withdrawal or disengagement, resulting in decreased interaction between the aging person and others in the social system he belongs to". The theory claims that it is natural and acceptable for older adults to withdraw from society. Psychological abuse of elders Death and the anxiety related to it, who’s at risk? Age and suicide risk in the different age groups? Geriatric Depression Screen- Geriatric Depression Scale: Short Form Choose the best answer for how you have felt over the past week: 1. Are you basically satisfied with your life? YES / NO 2. Have you dropped many of your activities and interests? YES / NO 3. Do you feel that your life is empty? YES / NO 4. Do you often get bored? YES / NO 5. Are you in good spirits most of the time? YES / NO 6. Are you afraid that something bad is going to happen to you? YES / NO 7. Do you feel happy most of the time? YES / NO 8. Do you often feel helpless? YES / NO 9. Do you prefer to stay at home, rather than going out and doing new things? YES / NO 10. Do you feel you have more problems with memory than most? YES / NO 11. Do you think it is wonderful to be alive now? YES / NO 12. Do you feel pretty worthless the way you are now? YES / NO 13. Do you feel full of energy? YES / NO 14. Do you feel that your situation is hopeless? YES / NO 15. Do you think that most people are better off than you are? YES / NO Answers in bold indicate depression. Score 1 point for each bolded answer. A score 5 points is suggestive of depression. A score ≥ 10 points is almost always indicative of depression. A score 5 points should warrant a follow-up comprehensive assessment. Geriatric Depression Scale The Geriatric Depression Scale (GDS) was specifically developed for use in geriatric populations, originally as a 30-item scale. It was modified a 15-item scale, which has been widely used. The GDS was later reduced to 5 items, so as to be better received by elderly patients. The questions elicit only “yes” or “no” responses, making comprehension easier compared with multiple-choice answers. The 5-item scale has a sensitivity of 94%, specificity of 81%, and demonstrated a significant agreement in the clinical diagnosis of depression with the 15-item scale. The 5-item scale is scored by 1 point for a “no” answer on the first question or a “yes” answer for the remaining questions. A score of greater than or equal to 2 is a positive screen for depression Which of the following is not an indication for use of a serotonin-norepinephrine reuptake inhibitor?- Unresponsiveness to an SSRI Lucy Garcia is a 42-year-old Hispanic female with a 20-plus-year history of depression. She is currently hospitalized for treatment of progressive, acute-on-chronic depressive symptoms, including refusal to get out of bed and inattentiveness to personal hygiene.------Electroconvulsive treatments Which of the following are risk factors for obesity? (Select all that apply.----- African American and Hispanic youth are at increased risk for childhood and adolescent obesity, Skipping breakfast Frequent takeout/fast-food meals, Consumption of sugar sweetened beverages How should a physician assess the risk for suicide in a depressed adolescent? (Select all that apply.) By asking family members whether they feel that the patient is at risk for suicide By establishing a no-suicide contract with depressed adolescents Why must a physician assess the risk for suicide in a depressed adolescent? All suicide gestures should be taken seriously WEEK 3 ENT Colyar, M. R. (2015). Advanced practice nursing procedures. Philadelphia, PA: F.A. Davis Company.   • Section 5, “Head: Eyes, Ears, Nose, and Mouth” o Chapter 68, “Audiometry Testing”- C/O tinnitus, unexplained behavior changes in geriatrics, contraindications (cerumen obstruction, otitis externa) pull the pinna up and back, normal -10-26 dB, mild 20-40 dB, mod. 56-70 dB, profound 91 dB o Chapter 70, “Tympanometry” – test mobility of tympanic membrane, middle ear pressure, and volume of the external canal. Used to measure otitis media resolution, serous otitis media, presence of eustachian tube dysfunction problems and screen for developemental delays. The tympanometer measures the "admittance" or "compliance" of the tympanic membrane while different pressures are being applied to the external ear canal.TM is measured in cubic centimeters, and the pressure in the ear canal is measured in decapascals (daPa). If the middle ear space is filled with fluid, most of the sound is reflected back to the probe from the stiff tympanic membrane. If the middle ear space is filled with air, and the ossicles are intact, energy is absorbed by the tympanic membrane, ossicles, and inner ear structures. The tracing will read "normal". If there is disruption of the ossicles, or if a portion of the TM is flaccid, a large amount of energy will be absorbed into the TM and the tracing will display an abnormally peaked compliance. Chapter 71, “Visual Function: Evaluation (Snellen, Illiterate E) Procedures—Eyes” o Chapter 76, “Eyebrow Laceration Repair”-may consider suturing beyond the 6 hr postlac time d/t cosmetic reasons, above and below eyebrow may be close d with steri stripes if less than 0.25 cm in length (poor cosmetic healing), contraindications (involves intramarginal lid of the eye, greater than 12 hrs old, global injury or orbit fx) suture, appy topical antibiotic ointment, light pressure dressing remove in 24 hrs, remove in 3-5 days, no PO antibiotics can use topical antibiotics) Tylenol for pain o Chapter 77, “Eyelid Eversion Procedures: Ears/Nose” pt look down use cotton tip applicator to flip eye lid up, then have pt look up to return to normal o Chapter 79, “Cerumen Impaction Removal: Irrigation of the Ear and Curette Technique” Curette technique for easily visualized wax, irrigation (mix hydrogen peroxide and H2O room temp (cold or to warm can cause vertigo) don’t direct toward tympanic membrane , after removal dry ear canal with alcohol applied to a cotton applicator, home remadies instill 2 drops of warmed mineral or glycerin or over counter agents 4x a day for 4 days, return to office o Chapter 80, “Ear Piercing” o Chapter 88, “Tooth Avulsion and Fracture” Papadakis, M. A., McPhee, S. J., & Rabow, M. W. (2018). Current medical diagnosis & treatment (57th ed.). New York, NY: McGraw Hill.   • Chapter 7, “Disorders of the Eyes & Lids” (pp. 170-204) • Chapter 8, “Ear, Nose, & Throat Disorders” (pp. 205-245) Weber, E. C., Vilensky, J. A., & Fog, A. M. (2013). Practical radiology: A symptom-based approach. Philadelphia, PA: F.A. Davis Company.   • Chapter 5, “EENT Imaging” (pp. 105–123) EENT EYE • Cornea: clear front window of the eye that transmits and focuses light into the eye. • Iris: colored part of the eye that helps regulate the amount of light that enters • Posterior chamber region behind the iris • Anterior chamber region between the cornea and iris • Pupil: dark aperture in the iris that determines how much light is let into the eye • Lens: transparent structure inside the eye that focuses light rays onto the retina • Retina: nerve layer that lines the back of the eye, senses light, and creates electrical impulses that travel through the optic nerve to the brain • Macula: small central area in the retina that contains special light-sensitive cells and allows us to see fine details clearly • Optic nerve: connects the eye to the brain and carries the electrical impulses formed by the retina to the visual cortex of the brain • Vitreous: clear, jelly-like substance that fills the middle of the eye Eye pressure is measured in millimeters of mercury (mm Hg). Normal eye pressure ranges from 12-22 mm Hg, and eye pressure of greater than 22 mm Hg is considered higher than normal. When the IOP is higher than normal but the person does not show signs of glaucoma, this is referred to as ocular hypertension. Eye pain from medications- Ophthalmic solutions risk for contamination are preservative free solutions like tetracaine, proparacaine, fluorescein. Most dangerous is fluorescein D/T contamination with P aeruginosa which can rapidly destroy the eye. Store preservative -free in the refrig, trash after 1 week of opening. Eye trauma -use freshly open bottles or single use products. Long term topical eye therapy patient may develop hypersensitivity reaction to active ingredients or preservative. To avoid systemic reaction use 1-2 drops at a time and few minutes of nasolacrimal occlusion or eyelid closure. Preventative free for glaucoma treatment and contact lens solutions * Cataract Familiarize yourself with Cataracts, presentation? TRX?- REFER TO OPTHO WHEN VISION LOSS EFFECT ACTIVITIES OF DAILY LIVING/ Complications Serious complications of cataract surgery include retinal detachment and endophthalmitis You develop them when protein builds up in the lens of your eye and makes it cloudy. This keeps light from passing through clearly. It can cause you to lose some of your eyesight decreased visual acuity, gradual progressive blurred vision, no pain or redness, lens opacities may be grossly visible. They are opacities of the crystalline lens and ae usually bilateral, leading cause of blindness, congenital, (owing to intrauterine infections, rubella/CMV, traumatic, secondary to disease (diabetes, myotonic dystrophy, atopic dermatitis, corticosteroid use, uveitis, radiation, statin drugs, smoking increase the risk, vitamins/antioxidants may prevent. Complaints of glare with bright light or night driving, cataract can be seen with a dilated pupil, Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development.[38][39] While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements;[23] though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin.[40][41][42] Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.[ TREATMENT - Cataract removal can be performed at any stage and no longer requires ripening of the lens. Surgery is usually 'outpatient' and performed using local anesthesia. About 9 of 10 patients can achieve a corrected vision of 20/40 or better after surgery.[34] Several recent evaluations found that cataract surgery can meet expectations only when significant functional impairment due to cataracts exists before surgery. Visual function estimates such as VF-14 have been found to give more realistic estimates than visual acuity testing alone.[34][44] In some developed countries, a trend to overuse cataract surgery has been noted, which may lead to disappointing results.[45] Phacoemulsification is the most widely used cataract surgery in the developed world.[46][47] This procedure uses ultrasonic energy to emulsify the cataract lens. Phacoemulsification typically comprises six steps: • Anaesthetic – The eye is numbed with either a subtenon injection around the eye (see: retrobulbar block) or topical anesthetic eye drops. The former also provides paralysis of the eye muscles. • Corneal incision – Two cuts are made at the margin of the clear cornea to allow insertion of instruments into the eye. • Capsulorhexis – A needle or small pair of forceps is used to create a circular hole in the capsule in which the lens sits. • Phacoemulsification – A handheld ultrasonic probe is used to break up and emulsify the lens into liquid using the energy of ultrasound waves. The resulting 'emulsion' is sucked away. • Irrigation and aspiration – The cortex, which is the soft outer layer of the cataract, is aspirated or sucked away. Fluid removed is continually replaced with a saline solution to prevent collapse of the structure of the anterior chamber (the front part of the eye). • Lens insertion – A plastic, foldable lens is inserted into the capsular bag that formerly contained the natural lens. Some surgeons also inject an antibiotic into the eye to reduce the risk of infection. The final step is to inject salt water into the corneal wounds to cause the area to swell and seal the incision. Extracapsular cataract extraction (ECCE) consists of removing the lens manually, but leaving the majority of the capsule intact.[48] The lens is expressed through a 10- to 12-mm incision which is closed with sutures at the end of surgery. ECCE is less frequently performed than phacoemulsification, but can be useful when dealing with very hard cataracts or other situations where emulsification is problematic. Manual small incision cataract surgery (MSICS) has evolved from ECCE. In MSICS, the lens is removed through a self-sealing scleral tunnel wound in the sclera which, ideally, is watertight and does not require suturing. Although "small", the incision is still markedly larger than the portal in phacoemulsion. This surgery is increasingly popular in the developing world where access to phacoemulsification is still limited. Intracapsular cataract extraction (ICCE) is rarely performed.[49] The lens and surrounding capsule are removed in one piece through a large incision while pressure is applied to the vitreous membrane. The surgery has a high rate of complications. The postoperative recovery period (after removing the cataract) is usually short. The patient is usually ambulatory on the day of surgery, but is advised to move cautiously and avoid straining or heavy lifting for about a month. The eye is usually patched on the day of surgery and use of an eye shield at night is often suggested for several days after surgery.[12] In all types of surgery, the cataractous lens is removed and replaced with an artificial lens, known as an intraocular lens, which stays in the eye permanently. Intraocular lenses are usually monofocal, correcting for either distance or near vision. Multifocal lenses may be implanted to improve near and distance vision simultaneously, but these lenses may increase the chance of unsatisfactory vision Herpes zoster- affects the trigeminal nerve, malaise, fever, periorbital burning and itching Hordeolum-staphylococcal abscess red/tender/swollen area upper or lower eye lid, warm compresses/ bacitracin or erthy ointment, not better in 48 hrs incision may need to be done Chalazion-granulomatous inflammation of the Meibomian gland, hard/nontender swelling on the upper and lower lids Blepharitis-chronic bilateral inflammatory condition of the lid margins Entropion-inward turning of lower lid Ectropion-outward turning of the lower lid Vitreous hemorrhage- sudden visual loss, floaters, bleeding within the eye, caused by retinal tear, diabetic retinopathy, retinal vein occlusion, retinal vasculitis * Dacrocystitis- an infection of the lacrimal sac, due to congenital or acquired obstruction of the nasolacrimal system, acute or chronic in peds and age over 40, unilateral, staphylococcus aureus and streptococci in acute dacryocystitis and staphylococcus epidermidis, streptococci, or gram-negative bacilli in chronic dacrocystitis. ACUTE is characterized by pain, swelling, tenderness, and redness in the tear sac area, may have purulent material, systemic antibiotics, surgery. CHRONIC tearing and discharge are the primary signs (mucus and pus), antibiotics, relive the obstruction (surgery of the lacrimal sac/formation of fistula into the nasal cavity, nasolacrimal intubation or balloon). Congenital usually resolve spontaneously. • What is acute angle glaucoma? – (ACUTE ANGLE-CLOSURE CRISIS ESSENTIAL S AGE GROUP/ FARSIGHTED/RAPID ONSET OF SEVER PAIN/PROFOUND VISUAL LOSS/HALOS AROUND LIGHTS/RED EYE/ CLOUDY CORNEA/DIALATED PUPIL/ HARD ON PALPATION/ MAY HAVE NAUSEA & ABD PAIN. Visual field and decreased visual acuity, PRIMARY -closure of the preexisting narrow anterior chamber angle, precipitated by pupil dilatation (can occur from sitting in a dark theater, stress, meds anticholinergics, bronchodilators, atropine, antidepressants, antispasmodics, nasal decongestants) common in Inuits and Asians. SECONDARY does not require a preexisting narrow angel, occur in anterior uveitis or dislocation of the lens due to drug, SYMPTOMS SAME AS PRIMARY difference is in management, associated with hemodialysis, TREATMENT IS REDUCTION OF INTRAOCULAR PRESSURE WITH A SINGLE 500 MG iv DOSE OF ACETAZOLAMIDE, FOLLOWED BY 250 MG ORALLY 4 X DAY WITH TOPICAL ONITMENT/OSMOTIC DIURETICS SUCH AS ORAL GLYCERIN AND IV UREA OR MANNITOL ALL DOSED AT 1-2 G/KG MAYBE USED IF ACETAZOLAMIDE DOESNOT WORK ONCE PRESSURE DECREASES FOR PRIMARY ACUTE ANGLE GLACOMA TOPICAL 4% PILOCARPINE 1 DROP EVERY 15 MINUTES FOR 1 HOUR THEN 4 TIMES A DAY/ FAILURE OF TREATMENT MAY NEED SURGICAL CORNEAL INDENTATION LASER TREATMENT ALL PATIENTS SHOULD UNDERGO PROPHYLATIC LASER PERIPHERAL IRIDOTOMY TO THE UNAFFECTED EYE. SECONDARY ADDED TX IS DETERMINED BY THE CAUSE IF NOT TREATED IN 2-5 DAYS PERMANET VISUAL LOSS (MUST REF EMERGENTLY TO AN OPTHALMOLOGIST) • Chronic uveitis medication management- INTRAOCULAR INFLAMMATION, PRIMARYLY IMMUNOLOGIC/DISORDERS ASSOCIATED ARE ANKYLOSING SPONDYLITID, REACTIVE ARTHRITIS, PSORIASIS/ UC AND CROHNS (ALL THES ARE HLA-B27) HERPES SIMPLEX/ZOSTER CAN CAUSE NONGRANULOMATUS ANTERIOR UVETITIS, vision blurred, mod. Pain, cornea clear, pupil size small, pupil response poor, intraocular pressure usually normal can be elevated, no organisms/ TREATMENT FOR ANTERIOR UVETITIS TOPICAL STEROIDS,DILATATION OF THE PUPIL IS IMPORTANT TO RELIEVE DISCOMFORT, POSTERIOR -TREATMENT SYSTEMIC PERIOCULAR OR INTRAVITREAL CORTICOSTERIODS (AZATHIOPRINE, CYSLOSPORINE, MYCOPHENOLATE, METHOTREXATE, TACROLIMUS, SIROLIMUS (BIOLOGIC THERAPHY/INTRACULAR INJECTION) INFECTIOUSE CAUSE USE ANTIBIOTICS NO NEED FOR PUPIL DILITATION, POSTERIOR IS WORSE THAN ANTERIOR/REFER URGENTLY TO OPTHO, ERGENT WITH VISUAL LOSS, ADMIT FOR SEVERE UVEITIS AND THOSE NEEDING IV THERAPHY • Gonococcal conjunctivitis presentation and medication management-contact from infected genital secretions, copious discharge, OPTHOMOLOGY EMERGENCY, stained smear and culture of discharge, 1 gram of IM ceftriaxone, topical may be added (bacitracin/ erythromycin) • Trachoma (chlamydial Kertoconjuctivitis -most common infections to cause blindness • Dry eye (Keratoconjunctivitis Sicca) loss of aqueous component of tears • Allergic conjunctivitis- itchy, tearing, redness, stringy discharge, occasional photophobia and vision loss • Viral, allergic, bacterial conjunctivitis: CORNEA CLEAR, PUPIL NORMAL, LIGHT RESPONSE NORMAL, INTRAOCULAR PRESSURE NORMAL know presentations and trx- Conjunctivitis most common eye disease, acute / chronic. VIRAL – adenovirus is the most common cause Bilaterally/copious discharge/FB sensation to eye/follicular conjunctivitis. Adenovirus type 8,19, 37 causes keratoconjunctivitis results in vision loss, lasts about 2 weeks. Adenovirus type 3,4,7 and 11 is associated with pharyngitis, fever, malaise and preauricular adenopathy (pharyngoconjunctival fever) last 10 days. VIRAL- due to herpes, unilateral, lid vesicles, and enterovirus 70 or coxsackievirus A24 (acute hemorrhage) No treatment for viral cold compresses/ topical sulfonamides to prevent secondary infections, Viral from HERPES use topical ganciclovir 0.15% gel and or oral acyclovir 3% 5x day. BACTERIAL- cause staph, MRSA, S pneumoniae, haemophilus, , copious purulent discharge, severe cases obtain culture to r/o gonococcal, last 10-14 days, topical sulfonamide or oral antibiotics. Macular degeneration presentation and S&S, trx - is a common eye condition and a leading cause of vision loss among people age 50 and older. It causes damage to the macula, a small spot near the center of the retina and the part of the eye needed for sharp, central vision, which lets us see objects that are straight ahead. In some people, AMD advances so slowly that vision loss does not occur for a long time. In others, the disease progresses faster and may lead to a loss of vision in one or both eyes. As AMD progresses, a blurred area near the center of vision is a common symptom. Over time, the blurred area may grow larger or you may develop blank spots in your central vision. Objects also may not appear to be as bright as they used to be. AMD by itself does not lead to complete blindness, with no ability to see. However, the loss of central vision in AMD can interfere with simple everyday activities, such as the ability to see faces, drive, read, write, or do close work, such as cooking or fixing things around the house. The Macula The macula is made up of millions of light-sensing cells that provide sharp, central vision. It is the most sensitive part of the retina, which is located at the back of the eye. The retina turns light into electrical signals and then sends these electrical signals through the optic nerve to the brain, where they are translated into the images we see. When the macula is damaged, the center of your field of view may appear blurry, distorted, or dark. Who is at risk? Age is a major risk factor for AMD. The disease is most likely to occur after age 60, but it can occur earlier. Other risk factors for AMD include: • Smoking. Research shows that smoking doubles the risk of AMD. • Race. AMD is more common among Caucasians than among African-Americans or Hispanics/Latinos. • Family history and Genetics. People with a family history of AMD are at higher risk. At last count, researchers had identified nearly 20 genes that can affect the risk of developing AMD. Many more genetic risk factors are suspected. You may see offers for genetic testing for AMD. Because AMD is influenced by so many genes plus environmental factors such as smoking and nutrition, there are currently no genetic tests that can diagnose AMD, or predict with certainty who will develop it. The American Academy of Ophthalmology (link is external) currently recommends against routine genetic testing for AMD, and insurance generally does not cover such testing. Does lifestyle make a difference? Researchers have found links between AMD and some lifestyle choices, such as smoking. You might be able to reduce your risk of AMD or slow its progression by making these healthy choices: • Avoid smoking • Exercise regularly • Maintain normal blood pressure and cholesterol levels • Eat a healthy diet rich in green, leafy vegetables and fish How is AMD detected? The early and intermediate stages of AMD usually start without symptoms. Only a comprehensive dilated eye exam can detect AMD. The eye exam may include the following: • Visual acuity test. This eye chart measures how well you see at distances. • Dilated eye exam. Your eye care professional places drops in your eyes to widen or dilate the pupils. This provides a better view of the back of your eye. Using a special magnifying lens, he or she then looks at your retina and optic nerve for signs of AMD and other eye problems. • Amsler grid. Your eye care professional also may ask you to look at an Amsler grid. Changes in your central vision may cause the lines in the grid to disappear or appear wavy, a sign of AMD. • Fluorescein angiogram. In this test, which is performed by an ophthalmologist, a fluorescent dye is injected into your arm. Pictures are taken as the dye passes through the blood vessels in your eye. This makes it possible to see leaking blood vessels, which occur in a severe, rapidly progressive type of AMD (see below). In rare cases, complications to the injection can arise, from nausea to more severe allergic reactions. • Optical coherence tomography. You have probably heard of ultrasound, which uses sound waves to capture images of living tissues. OCT is similar except that it uses light waves, and can achieve very high-resolution images of any tissues that can be penetrated by light—such as the eyes. After your eyes are dilated, you’ll be asked to place your head on a chin rest and hold still for several seconds while the images are obtained. The light beam is painless. During the exam, your eye care professional will look for drusen, which are yellow deposits beneath the retina. Most people develop some very small drusen as a normal part of aging. The presence of medium-to-large drusen may indicate that you have AMD. Another sign of AMD is the appearance of pigmentary changes under the retina. In addition to the pigmented cells in the iris (the colored part of the eye), there are pigmented cells beneath the retina. As these cells break down and release their pigment, your eye care professional may see dark clumps of released pigment and later, areas that are less pigmented. These changes will not affect your eye color. Currently, no treatment exists for early AMD, which in many people shows no symptoms or loss of vision. Your eye care professional may recommend that you get a comprehensive dilated eye exam at least once a year. The exam will help determine if your condition is advancing. As for prevention, AMD occurs less often in people who exercise, avoid smoking, and eat nutritious foods including green leafy vegetables and fish. If you already have AMD, adopting some of these habits may help you keep your vision longer. Diabetic retinopathy People with diabetes can have an eye disease called diabetic retinopathy. This is when high blood sugar levels cause damage to blood vessels in the retina. These blood vessels can swell and leak. Or they can close, stopping blood from passing through. Sometimes abnormal new blood vessels grow on the retina. All of these changes can steal your vision. non-proliferative diabetic retinopathy) This is the early stage of diabetic eye disease. Many people with diabetes have it With NPDR, tiny blood vessels leak, making the retina swell. When the macula swells, it is called macular edema. This is the most common reason why people with diabetes lose their vision Also with NPDR, blood vessels in the retina can close off. This is called macular ischemia. When that happens, blood cannot reach the macula. Sometimes tiny particles called exudates can form in the retina. These can affect your vision too. If you have NPDR, your vision will be blurry. PDR (proliferative diabetic retinopathy) PDR is the more advanced stage of diabetic eye disease. It happens when the retina starts growing new blood vessels. This is called neovascularization. These fragile new vessels often bleed into the vitreous. If they only bleed a little, you might see a few dark floaters. If they bleed a lot, it might block all vision. These new blood vessels can form scar tissue. Scar tissue can cause problems with the macula or lead to a detached retina. PDR is very serious, and can steal both your central and peripheral (side) vision. • Open angle glaucoma- usually bilaterally/optic disk cupping/genetic/ ESSENTIAL NO SYMPTOMS EARLY ON, BILATERAL LOSS OF PERIPHERAL VISION/CUPPING OPTIC DISC/INCREASED INTRAOCULAR PRESSURE, acute angle closure glaucoma is an immediate referral to optho. ) In open-angle glaucoma, the angle in your eye where the iris meets the cornea is as wide and open as it should be, but the eye’s drainage canals become clogged over time, causing an increase in internal eye pressure and subsequent damage to the optic nerve. It is the most common type of glaucoma/ In open angle glaucoma, the drainage canal of the eye called the trabecular meshwork is not anatomically blocked. We explain to our patients that open angle glaucoma is like a clogged drain. The drainage canal becomes clogged and allows less fluid to leave the eye. The eye continues to make fluid in the ciliary body and therefore, the pressure in the eye starts to rise. Over time, a high pressure in the eye causes optic nerve damage. Vision loss in open angle glaucoma starts with the far peripheral vision. The dangerous thing about open angle glaucoma is that it is painless and if you do not get regular eye exams, significant damage can occur without the patient noticing. Open angle glaucoma runs in families and is usually treated with eye drops to lower the pressure. Our board certified eye doctors also use a laser called Selective Laser Trabeculoplasty (SLT) to lower the intraocular pressure. With SLT, a cold laser is used to safely open the drainage canal of the eye and lower the intraocular pressure. For those patients that are not well controlled with eye drops or do not want to use eye drops, SLT is a great way to lower the pressure in the eye. However, at times it is necessary to do more conventional surgery to lower the eye pressure. • Metal FB in eye, how do you evaluate and how do you remove? Do visual acuity first LEAVE A RUST RING, REQUIRES EXCISION OF THE AFFECTED TISSUE AND IS BEST DONE UNDER LOCAL ANESTHESIA USING A SLIT LAMP • Penetrating eye injury treatment-complication facial fx and loss of vision, avoid pressure may cause rupture and loos of vitreous humor (results in blindness), don’t not preform fluorescein stain if suspected globe injury, for exam donut ring with 4inch gauze, apply antibiotic ointment, place cup on top of gauze • Corneal abrasions: eval, presentation, medications (tetracaine onset 25 sec & 15 min duration, erythromycin or gentamicin/tobex , teaching, follow up/referral? – trauma to the anterior globe of the eye, only remove superficial foreign bodies, perform visual acuity, pupil response, visualize and inspect the orbital rim, verify equivocal sensation to orbit rim, corneal reflex (cotton wisp test), assess for subconjunctival hemorrhage, infection. EYE exam inspects anterior globe for clarity, hyphema, red reflex, lens opacity, vitreous and optic disc appearance, retinal abnormalities. Emergent referral for chemical acid or alkali exposure, flush with 0.9% NS for 15 minutes or 2 liters, to assess for abrasion use woods lamp, instill fluorescein drops, appears bright yellow or yellow green with woods lamp, irrigate vigorous with NS solution, if abrasion present apply topical antibiotics, apply eye patch FB removal not superficial use 27-25 gauge needle bevel side up, after removing any FB check for corneal abrasion, instructions no driving, eye patch no longer than 48 hrs or amblyopia (lazy eye), tentus if not within 5 years, Tylenol with codeine 24hrs then palin Tylenol, avoid all topical ophthalmic anesthetic and nonsteroidal d/t retardation in healing can occur, no rubbing eye, return 24-48 hrs, return sooner for increased pain, drainage, loss of vision Corneal infection: early signs is manifested by a white necrotic area around the crater and a small amount of gray exudate. Refer to opthomologist • Orbital cellulitis: presentation, S&S -FEVER, PROPTOSIS, RESTRICTION OF EXTRAOCULAR MOVEMENTSAND SWELLING WITH REDNESS OF THE LIDS. IMMEDIATE TREATMENT WITH IV ANTIBIOTICS TO PREVENT OPTIC NERVE DAMAGE AND SPREAD OF INFECTION TO THE CAVERNOUS SINUSES/MENINGES AND BRAIN. CAUSE INFECTION OF THE PARANASAL SUNUSES/ ORGANISMS ARE S pneumoniae, treatment with penicillinase-resistant penicillin’s such as nafcillin or together with metronidazole or clindamycin to treat anaerobic infections. If trauma is the cause use cephalosporin such as cefazolin or ceftriaxone, MRSA use vanco or clindamycin. Surgery may be required . ALLERGY TO PCN USE VANCO, LEVOFLOXACIN, METRONIDAZOLE. IF IMMUCOMPROMIZED CONSIDER USING ZYGOMYCOSIS, REF TO OPTHO EMERGENTLY • Orbital fractures: patho and causes, teaching for post-op/or discharge? Orbital fractures are commonly seen with midfacial trauma. Eye trauma, car accident or abuse. increased intraorbital pressure causes a decompressing fracture into an adjacent sinus. The Buckling theory contends that the posterior transmission of a direct orbital rim force causes a buckling and resultant fracture of the orbital wall. Both mechanisms may be involved to various degrees to produce orbital blow-out fractures. Orbital tissue (fat, fibrous septa, extraocular muscle) may be involved with the fracture site, resulting in ocular motility disturbance, while volume augmentation leads to globe malpositioning. Initial treatment in patients with facial injuries should be aimed at airway security, hemodynamic stability, and cervical-spine integrity. Head injuries must be ruled out. The patient should be evaluated for additional soft-tissue and bony injuries of the head and neck. The importance of recording visual acuity cannot be overemphasized/periocular ecchymosis and edema are present, position of the globe needs assessing. Patients should avoid blowing their nose and performing Valsalva maneuvers to limit intraorbital emphysema. • Visual loss with acute orbital emphysema has been reported. • Oral antibiotic therapy may be considered. Fractures that involve the medial wall and floor may be considered open fractures, as laceration of the sinus mucosa is inevitable. • Analgesia and antiemetics may be required. • The use of oral steroids (prednisone 1 mg/kg/d) has been advocated to decrease soft-tissue edema. EAR Different types of hearing loss and why they occur- Conductive/Sensorineural Conductive hearing loss is from external or middle ear dysfunction, a decrease in sound vibration to the inner ear 1. Obstruction (wax), 2. Mass loading (middle ear effusion) 3. Stiffness (otosclerosis- a hereditary disorder causing progressive deafness due to overgrowth of bone in the inner ear) 4. Discontinuity (ossicular disruption) . Most common ear wax and transient Eustachian tube disfunction from upper respiratory infection. Persistent conductive loss D/T chronic ear infections, trauma, or otosclerosis. Corrected with medical or surgical treatment Sensorineural hearing loss- deterioration of cochlea, loss of hair cells, gradually progressive, high frequency loss with advanced age, other causes excessive loud noises head trauma and diseases, not correctable. Sudden loss can be treated with corticosteroids if given within several weeks of onset. Neural hearing loss involve the 8th cranial nerve (causes acoustic neuroma, MS and auditory neuropathy) Weber Test – tuning fork on forehead, top of head, front teeth. In conductive loss the sound appears louder in the poorer hearing ear, with sensorineural radiates to better ear. Rinne Test tuning fork on mastoid bone and in front of the ear canal. In Conduction bone exceeds air conduction; In Sensorineural the opposite is true Acute otitis media: causes, trx, presentation- Otalgia, erythema and hypomobility of tympanic membrane, pressure, decreased hearing, fever, mastoid tenderness (ruptured of tympanic membrane is accompanied by sudden decrease in pain and followed by otorrhea) usually follows or is with a upper respiratory infection, bacterial eustachian tube obstruction with fluids and mucous, most common bacteria Streptococcus pneunomiae, haemophilus influenzae, streptococcus pyogenes. TX- antibiotics and nasal decongestions , first line amoxicillin 80-90mg/kg/day divided twice a day, or erthyro 50mg/kg/day, sulfonamide 150mg/kg/day Reoccurring infection treat with sulfamethoxazole 500mg or amoxicillin 250mgor 500mg 1 dose per day for 1-3 months. Vertigo, how do you evaluate and trx? Spinning, Peripheral( onset is sudden, tinnitus and hearing loss, horizontal nystagmus may be present, unable to walk or stand, nausea / vomiting, causes labyrinths/Meniere disease (inner ear disorder)/ benign postural vertigo/ etoh/ inner ear .( evaluate the ears, eye moments, cranial nerve testing and Romberg test) Central – onset is gradual, no auditory symptoms, nystagum not always present, episodic events can occur due to diplopia, cerebral lesions involving the temporal cortex can cause vertigo, evaluate with audiogram/ electronystagmography or videonystagmography and head MRI (seizures, MS,) Side effect of medications Labyrinthitis-acute onset of continues vertigo lasting days or week, unk cause, hearing loss and tinnitus, if febrile or symptoms of infection give antibiotics, meclizine Epistaxis: causes, trx, what to look for in complications? Infection? Causes-trauma, nose picking, FB, nose blowing, rhinitis, dry MM, nasal O2, deviated septum, atherosclerotic disease, cocaine, osler-weber-rendu syndrome, etoh. Anterior bleeding direct pressure, sitting position, leaning forward, 1-2 sprays of decongestant (phenylephrine 0.125-1%) , if bleeding doesn’t stop use cocaine 4% or teracaine/lidocaine POSTERIOR bleeds associated with atherosclerotic dx and hypertension Reduce the risk of toxic shock syndrome when packing is in palce give CEPHALEXIN 500MG 4X DAY OR CLINDAMYCIN 150 MG 4X DAY Complications: Nasal Packing A. Septal Hematoma or abscess 1. Avoid excessive Trauma on Nasal Packing insertion B. Septal pressure necrosis 1. Avoid overly tight Nasal Packing C. Risk of Sinusitis or Toxic Shock Syndrome 1. Apply Bactroban Topical Ointment in nares 2. Oral antibiotic prophylaxis indications are patient specific a. Optional in otherwise healthy patients b. Recommended if SBE Prophylaxis would otherwise be indicated c. Amoxicillin at standard treatment doses is reasonable option d. Derkay (1989) Arch Otolaryngol Head Neck Surg 115: 439-441 [PubMed] e. Bandhauer (2002) Am J Rhinol 16(3): 135-139 [PubMed] IV. Preparation: Local Anesthetic and Topical Decongestant A. Lidocaine 2% and Phenylephrine 4% mix 1:1 on cotton or B. Afrin and Cetacaine sprayed into nare separately V. General A. Gown prior to Nasal Packing (bloody procedure) B. Use topical Bactroban in nares with packing C. Remove non-absorbable nasal packs after 2-3 days 1. Prolonged Nasal Packing has been associated with Toxic Shock Syndrome 2. Jacobson (1986) Arch Otolaryngol Head Neck Surg 112: 329-32 [PubMed] D. The packing tip should be barely visible in the posterior pharynx when the patient opens their mouth VI. Preparations: Nasal Packing options A. Rocket pack (Rhino Rocket) 1. Easiest of all methods and most common in Emergency Departments 2. Two lengths (short for anterior bleed, long for posterior or unknown) 3. Soak for 30 seconds in sterile water, insert and inflate B. Vaseline Gauze pack or 0.5 x 72 inch strips 1. Use Bayonet forceps with nasal speculum 2. Layer (accordion-fold) from bottom to top 3. Start each layer as far posterior as possible 4. Press down each layer before inserting next one C. Absorbable Gelatin foam (Gelfoam) D. Oxidized Cellulose (Surgicel) E. Nasal tampon (Merocel or Doyle sponge) 1. Easier to insert then gauze pack method 2. Gently insert along floor of nose 3. Expand with saline or Phenylephrine 4. Absorbable oxidized cellulose a. Effective for those on Anticoagulants b. Do not need to be removed (will absorb) VII. Patient Instructions A. Return for removal of non-absorbable packs in 2-3 days B. Apply Bactroban Topical Ointment in nares C. Avoid vasodilating actions 1. Physical exertion 2. Spicy foods 3. Alcohol D. Avoid Nasal manipulation or nose blowing E. Sneeze with mouth open F. Alleviate drying 1. Saline Nasal Sprays several times per day 2. Apply Bacitracin ointment qd to bid 3. Vaseline does not appear effective in children Bacterial sinusitis: treatment, presentation, when you suspect it, what is GOLD standard of dx testing… purulent yellow/green nasal discharge or expectoration, facial pain or pressure, cough, malaise, fever and headache, nasal obstruction, or congestion, dental pain, halitosis, a result of impaired mucociliary clearance and obstruction of the ostiomeatal complex or sinus pore, bacteria- S. pneumoniae, streptococci, H influenza, VIRAL VS BACTERIAL- BACTERAIL LAST LONGER THAN 10 DAYS FROM ONSET, acute last less than 4 weeks, subacute 4-12 weeks, most common maxillary (largest and with only 1 pathway for drainage) unilateral face fullness/tenderness/pressure over check/ incisor pain. Ethmoid (between the eyes radiate to orbits, nose) Sphenoid (headache middle of head), Frontal (forehead, below eyebrow, orbit rim) Hospital acquired from NGT TREATMENT-NSAIDS, ORAL PSEUDOEPHEDRINE 30-60MG Q 6 HRS MAX 240MG/DAY, NASAL METAZOLINE .05% 1-2 SPRAYS EACH NOSESTRIL Q6-8HRS UP TO 3 DAYS, INTRANASL CORTESTEROIDS, CONSIDER ANTIBIOTICS AFTER 10 DAYS OF SYMPTOMS, FIRST LINE ANTIBIOTICS IS AMOXICILLIN-CLAVULANATE 500MG/125 ORAL 3X DAY FOR 5-7 DAYS, OR 875MG/125 2X DAY 5-7 DAYS. IF ALLERGIC TO PCN THEN DOXY 100MG 2X DAY OR 200MG 2XDAY 5-7 DAYS. HOW TO DX-USUALLY MADE BY CLINICAL SYSMPTOMS, CT NOCONTRAST IF TUMOR OR OTHER OPPORTUNISTIC INFECTION SUSPECTED THEN MRI WITH GAD. Frontal Sinus Transillumination- put the ear scope light under the eyebrow cup your hand over the eye(light) and you should see a warm red glow Maxillary Sinus Transillumination- ask patient to tilt their head back and open their mouth place light source against the cheek below the eye a red glow on the hard palate indicates a normal air filled sinus Tonsillitis presentation- srtep concerns, (fever over 38c, anterior cervical adenopathy, lack of cough, pharyngotonsillar exudate) 2-3 symptoms still maybe strep. White purple exudate= mono DX- by swab culture or rapid antigen detection testing (RADT) Treatment- benzathine PCN or procaine PCN 1.2 million units IM or Penicillin V 250 mg 3x day or 500mg 2x day for 10days Complication scarlet fever Familiarize yourself with diagnostic studies for evaluation eye conditions in acute situations * Slit lamps, Snellen chart, Wood’s lamp Amsler grid- The Amsler grid, used since 1945, is a grid of horizontal and vertical lines used to monitor a person's central visual field. The grid was developed by Marc Amsler, a Swiss ophthalmologist. It is a diagnostic tool that aids in the detection of visual disturbances caused by changes in the retina, particularly the macula, as well as the optic nerve and the visual pathway to the brain. • Beta adrenergic antagonists: side effects • Cholinergic mimetics: side effects • Prostaglandin analogs: side effects • Osmotic diuretics: side effects Bells palsy: S&S, treatment, pain management- sudden onset of lower motor neuron facial palsy, may worsen over the following day or so, pain to ear, face feels stiff and pulled to one side, hyperacusis (debilitating hearing )or impaired taste may occur, no other neurologic changes, inflammatory reaction involving the facial nerve near the stylomastoid foramen or in the bony facial nerve, usually resolves without tx , but prednisone 60mg q day for 5 dyas then 25mg 2x day for 10 days, treat with acyclovir only if herpetic vesicles in external ear, eye drops to eye, may use eye patch if eye does not close Know epiglottis presentation, causes and treatment- rapid development of sore throat/odynophagia, bacterial or virus, H influenza, hospitalize for IV cefizoxime 1-2 g q 8-12 or cefuroxime 750-1000mg q 8hrs and dethamethasone 4-1- mg bolus than 4mg IV every 6 hrs Know cranial nerves and their function- Cardiovascular disorders • Chapter 10, “Heart Disease” (pp. 328-446) • Chapter 11, “Systemic Hypertension” (pp. 447-478) • Chapter 12, “Blood Vessel & Lymphatic Disorders” (pp. 479-506) • Chapter 28, “Lipid Disorders” (pp. ) ACS protocol: low risk vs high risk mi- use of statins and ASA, ace inhibitors. High intensity statin therapy (atorvastatin 40-80mg, rosuvastion 20 -40 mg) mod intensity. MOST patients with vascular disease in the absence of heart failure or LV dysfunction should be treated with an ACE Metabolic syndrome- (three or more of the following ) abdominal obesity, triglycerides 150mg/dl or high , HDL less than 40 for men, less than 50 for women, fasting glucose 110 or higher and hypertension. Contraindications to thrombolytic therapy in stroke and MIs- ST elevation in AVR = left main or three vessel diseases. When the there is not an ST elevation, hemorrhagic stroke MONA, what is it an when is it used? MONA is an acronym used to help medical professionals remember the initial treatment for acute coronary syndrome. MONA stands for morphine, oxygen, nitroglycerin and aspirin (“MONA greet chest pain patients at the door”). Duke criteria for infective endocarditis, presentation and treatment- Diagnostic : 2 Major Criteria and 0 Minor Criteria Diagnostic : 1 Major Criteria and 3 Minor Criteria Diagnostic : 0 Major Criteria and 5 Minor Criteria   Major Diagnostic Criteria Positive blood culture for typical Infective Endocarditis organisms (strep viridins or bovis, HACEK, staph aureous without other primary site, enterococcus), from 2 separate blood cultures or 2 positive cultures from samples drawn 12 hours apart, or 3 or a majority of 4 separate cultures of blood (first and last sample drawn 1 hour apart) Echocardiogram with oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or abscess, or new partial dehiscence of prosthetic valve or new valvular regurgitation Minor Diagnostic Criteria Predisposing heart condition or intravenous drug use Temp 38.0° C (100.4° F) Vascular phenomena: arterial emboli, pulmonary infarcts, mycotic aneurysms, intracranial bleed, conjunctival hemorrhages, Janeway lesions Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with endocarditis (excluding coag neg staph, and other common contaminants) Echocardiographic findings: consistent with endocarditis but do not meet a major criterion as noted above Heart murmurs: physical exams, grades of murmurs- Murmurs are sounds created by turbulent blood flow. They can occur at any time during the cardiac cycle. When you detect a murmur, you need to listen for a minute or more to determine its characteristics—the timing, pitch, quality, intensity, and pattern. You'll also want to identify where you hear it the loudest and if the sound radiates to other areas. To establish timing, focus on whether you hear the murmur continuously, during systole (after S1 and before S2) or d