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Neurological and Skin Conditions:
Diagnosis and Management
Multiple Sclerosis
Etiology of MS
More common in women than men More prevalent in Caucasians, especially those of Northern European descent Typically has an early onset, affecting individuals in their 20s to 40s Potential triggers include viral infections such as measles, herpes, chlamydia, and Epstein-Barr virus
Classification of MS
Relapsing-Remitting MS (RRMS) : Characterized by clearly defined episodes of relapse and recovery No progression between episodes, and patients typically return to their baseline
This is the most common initial presentation of MS
Secondary Progressive MS (SPMS) :
Begins as Relapsing-Remitting MS, but then progresses with or without occasional relapses
Patients do not return to their baseline between episodes, and the disease continues to worsen
Primary Progressive MS (PPMS) :
Characterized by a continuous and gradual progression of the disease, with minor improvements
Usually occurs after the age of 40 years
Progressive Relapsing MS (PRMS) :
Involves a progressive illness with clear relapses, and continued progression between relapses
Symptoms of MS
Relapsing-remitting episodes can include a variety of neurological symptoms, such as: Sensory disturbances (e.g., numbness, tingling)
Visual impairment (e.g., optic neuritis) Motor dysfunction (e.g., weakness, spasticity) Coordination and balance problems Cognitive impairment Fatigue Bladder and bowel dysfunction
Diagnosis of MS
Medical history and neurological examination Magnetic resonance imaging (MRI) of the brain and spinal cord to detect lesions Cerebrospinal fluid analysis to look for oligoclonal bands Evoked potentials (e.g., visual, auditory, somatosensory) to assess nerve conduction
Treatment of MS
Disease-modifying therapies (DMTs) to reduce the frequency and severity of relapses, and slow disease progression Examples: interferon beta, glatiramer acetate, fingolimod, natalizumab, ocrelizumab Symptomatic management of specific symptoms (e.g., spasticity, fatigue, bladder dysfunction) Rehabilitation (physical, occupational, and speech therapy) to maintain function and independence Supportive care and lifestyle modifications
Prognosis of MS
The course of MS is highly variable and unpredictable Relapsing-remitting MS generally has a better prognosis, with many patients experiencing long periods of remission Secondary progressive and primary progressive MS tend to have a more aggressive course, with gradual worsening of symptoms over time
Multiple Sclerosis (MS)
Malignant MS
Rapid onset and rapid deterioration
Benign MS
No deterioration after 10 years
Parkinson's Disease
Etiology
Neurodegenerative disorder caused by depletion of dopamine- producing cells Age of onset: 60 years More common in men than women More common in Caucasians Environmental (metals such as copper) and genetic factors (PARK gene)
Symptoms and Diagnostics
Classic triad: resting tremors, rigidity, and bradykinesia Motor symptoms: postural instability can cause falls Classic gait: diminished arm swing, shuffling steps, bent forward, and frozen gait Neuropsychiatric: depression, dementia, anxiety, psychosis, and sleep disruption Autonomic dysfunction: urinary incontinence, sexual dysfunction, constipation, and impaired thermoregulation Craniofacial: masked face/expressionless, dysphagia, impaired sense of smell, and drooling Diagnostic workup: H&P, CT, and MRI to assess for differential diagnoses
Parkinson's Treatment
Pharmacotherapy to relieve symptoms and improve functioning: Carbidopa-levodopa is the standard treatment Can experience on/off phenomena with working/not working of medications Add catechol-O-methyltransferase inhibitors Adequate nutrition Exercise
Dopaminergic Agents
Carbidopa-levodopa: Most effective drug, use with rasagiline May cause on/off phenomena, dyskinesia, confusion, headache, and hallucinations Dopamine agonists (pramipexole and ropinirole): May reduce risk for complications and alleviate symptoms May cause nausea, vomiting, dyskinesia, and confusion
MAO-B Inhibitors
Rasagiline: Adjunct therapy May cause serotonin syndrome, dyskinesia, arthralgia, and ataxia
Amyotrophic Lateral Sclerosis (ALS)
Etiology
Illness of motor neurons causing asymmetric weakness in upper or lower extremity Less likely to present with respiratory weakness, dysarthria, or dysphagia Onset age: 50 years More common in men Familial in 10% of cases Average survival: 2-5 years
Symptoms and Diagnostics
Progressive weakness over weeks/months Sensation intact Muscle atrophy Small muscle fasciculations Hyperreflexia Spasticity Serum CK elevated EMG: denervation Muscle biopsy: atrophic muscle fibers MRI: no abnormality
Management of ALS
Supportive and palliative: Immobility Altered respiratory function: ventilation and suction Dysphagia and poor nutrition Pain management Anxiety Medications: Riluzole can extend life by months but does not cure
Low Back Pain
Major Syndromes
Back strain Disk herniation Osteoarthritis/disk degeneration; osteophyte (bone spur) Spinal stenosis: narrowing spinal foramen leading to spinal nerve entrapment
Specific Pointers for Back Pain
Numbness Saddle anesthesia (cauda equina, mass)
Confusion Carotid bruit Vertebrobasilar artery syndrome: Bilateral visual disturbances Vertigo and ataxia Nausea and vomiting Drop attacks
TIA Diagnostics
Laboratory: CBC, PT, PTT/INR, electrolytes, lipid profile Imaging: CT: May reveal ischemia or infarct MRI: More sensitive than CT, preferred for vertebrobasilar TIA Duplex US: To identify carotid stenosis CT angiography: To evaluate neck and brain vessels (normal renal function required) MR angiography: Can assess vessels, good replacement for CTA Echocardiogram or Holter monitor for cardiac concern/assessment Transesophageal echocardiogram to assess aortic arch, left atrium, patent foramen ovale Cerebral angiography if candidate for carotid endarterectomy
TIA Management
Address underlying risk factors (hypertension, diabetes, hyperlipidemia, smoking, obesity) Carotid TIA: Surgery if more than 80% occluded, no surgery if less than 50% (can do stent then) Anticoagulation: Heparin, warfarin (PTT 1.5-2.5x patient's baseline), newer agents (Eliquis) Antiplatelet therapy: Aspirin or clopidogrel
Stroke
Etiology
Rapid onset of neurological deficit lasting longer than 24 hours, leading cause of disability Ischemic or hemorrhagic (80% ischemic) Risk factors: Hypertension Cardiac disease (atrial fibrillation) Smoking Obesity Hyperlipidemia (ischemic, low cholesterol hemorrhagic) Elderly Diabetes mellitus Alcohol and recreational drugs Female on contraception and smoking
Education on Stroke - Five 'Suddens'
Sudden weakness Sudden speech difficulty Sudden visual loss Sudden dizziness Sudden severe headache
Ischemic Stroke
Etiology
Thrombus in blood vessel in head or neck Predisposing factors: Atherosclerosis/hyperlipidemia Hypertension Diabetes mellitus Hypotension Smoking Trauma Atrial fibrillation, endocarditis, mitral stenosis (embolism)
Symptoms Based on Location
Middle cerebral artery: Hemiplegia (upper and face mostly), hemianesthesia, hemianopia Aphasia Neglect Anterior cerebral artery: Hemiplegia (lower mostly), primitive reflexes, confusion, behavioral changes if bilateral anterior Vertebral and basilar arteries: Loss of consciousness Vertigo Dysphagia, diplopia Ipsilateral cranial nerve deficits Contralateral sensory deficits Deep penetrating branches of major cerebral infarction (lacunar infarction): Associated with poorly controlled hypertension and diabetes Contralateral pure motor and sensory deficits Ipsilateral ataxia Dysarthria
Diagnostics
CT head without contrast initially, preferable to MRI to rule out hemorrhage Labs: CBC, PT, PTT/INR, lipid profile, drug screen, alcohol level ECG/Holter
Hemorrhagic Stroke
Etiology
Subarachnoid hemorrhage (SAH): Ruptured saccular aneurysm Arteriovenous malformation Intracerebral hemorrhage (ICH): Hypertension Predisposing factors: anticoagulants/thrombolytics, cocaine, alcohol, hematologic disorders
Symptoms
SAH
Sudden severe headache 'thunderclap headache' or 'worst headache of my life' Graded Hunt and Hess: 1: Asymptomatic 2: Moderate/severe headache, stiff neck, no focal deficits other than cranial nerve palsy 3: Drowsy, mild focal deficit 4: Stupor, hemiparesis 5: Deep coma, decerebration Graded Fisher: 1: No blood detected 2: Diffuse/vertical layers less than 1mm 3: Localized clot/vertical layer 1mm or more 4: Intracerebral/intraventricular clot with diffuse or no SAH
ICH
Hypertension Headache Vomiting (especially cerebellar) Basal ganglia: Eyes look to wound, reduced consciousness, contralateral hemiplegia Thalamic: Looking at nose, pinpoint pupils, coma, flaccid quadriplegia Cerebellar: Ipsilateral gaze paralysis, PERRLA, inability to stand/walk, facial weakness, gait ataxia, vertigo, dysarthria
Diagnostics
SAH
CT head: Ischemia or hemorrhage, sensitive in first 3 days, consider LP if smaller than 3mm and negative CT CSF: Bloody (103-106 RBC), xanthochromia (yellow, breakdown of blood)
CTA, prior to clot removal
ICH
CT without contrast to confirm bleed and determine size/site, may reveal structural abnormalities Cerebral angiography: Determine source as aneurysm or AVM MRI/MRA: Structural abnormalities Labs: CBC, PT/PTT, electrolytes, liver enzymes, kidney function
Management
SAH
ABC's May place external ventricular drain if hydrocephalus Bedrest strict Cardiac monitoring Treat headache, no NSAIDs (bleeding risk) No straining/exertion Stool softener Seizure prophylaxis (phenytoin or levetiracetam) Maintain SBP less than 160, may use nicardipine drip, labetalol push, hydralazine for bradycardia Cerebral edema: Mannitol or hypertonic saline Surgical clipping or coil ASAP Treat cerebral vasospasm Rebleeding: between day 2-19, repeat CT
ICH
ABC, intubate/give oxygen Control hypertension
Neurological Emergencies
Subarachnoid Hemorrhage (SAH) Management
SBP : 140 - 150, using medications like Nicardipine or Labetolol CPP : Maintain at 50 - 70 Pressors : If SBP less than 90, use Dopamine, Epinephrine, or Norepinephrine ICP : Maintain less than 20 Cerebral Edema : Treat with Mannitol for 5 days or less, monitoring serum osmolality. Alternatively, use 3% saline. Hydrocephalus : Treat with a ventricular drain Fluid Management : Maintain euvolemia Seizure Prophylaxis : Use Phenytoin or Levetiracetam Fever Control : Maintain normothermia
CSF analysis: Bacterial Meningitis: Cloudy appearance, elevated opening pressure (>180), increased WBCs (100-5000, predominantly polynuclear), increased protein (100-500), and decreased glucose (5-40) Viral Meningitis: Clear appearance, normal opening pressure (<180), increased WBCs (100-5000, predominantly mononuclear), normal or slightly increased protein (<200), and normal glucose (>45)
Meningitis Management
Antibiotics: 2-50 years: Vancomycin plus Ceftriaxone Older than 50 years: Vancomycin, Ampicillin, plus Ceftriaxone Meningococcal meningitis (college): Penicillin or Ceftriaxone if penicillin allergy Haemophilus influenzae: Ampicillin or Ceftriaxone Tuberculosis: Isoniazid plus Pyridoxine, Rifampin Streptococcus pneumoniae (infants): Add Dexamethasone Avoid hypotonic fluids Amphotericin B for fungal meningitis
Cerebral Abscess
Infected space-occupying lesion, from bacterial or fungal sources (sinusitis, lung infection, skin infection, trauma) Presentation: Ill-appearing/lethargic, signs of increased ICP (nausea/ vomiting, confusion/altered mental status) Stage 1: Headache, chills, fever, confusion, speech disorder Stage 2 (expanding cerebral mass): Symptoms and signs of a brain tumor (headache, confusion, drowsiness, stupor) Diagnostics: Increased WBC and ESR, LP (elevated opening pressure, mildly elevated protein), CT, and MRI (reveals necrosis vs. edema) Treatment: Antibiotics based on microbiology, and surgery/debridement when abscess is greater than 2.5cm
Encephalitis
Acute inflammation of the brain Most commonly caused by Herpes Simplex Virus, Tick Infestation, West Nile Virus, Toxoplasmosis (in AIDS patients), CMV, and Rabies Presentation: Lethargy, unstable vitals, nystagmus, photophobia, nausea/vomiting, nuchal rigidity, headache, and positive Babinski sign Diagnostics: CSF analysis (elevated WBC, normal/slightly elevated protein and glucose), EEG, IgM measurement in serum and CSF, CT, and MRI Treatment: IV fluids, respiratory and circulatory support, anticonvulsants, monitor for SIADH, Acyclovir for HSV, and report to CDC
Encephalopathy
Dysfunction of the brain caused by illness (process) Etiologies include Hepatic, Hypertensive, Metabolic, Hypercapnic, and Thiamine Deficiency (Wernicke) Presentation: Headache, altered mental status, confusion Diagnostics: Ammonia level, CSF analysis, EEG, and MRI Treatment: Address the underlying cause, provide supportive care, and use anticonvulsant therapy as needed
Seizures and Epilepsy
Seizure: Abnormal neuronal discharge within the brain Epilepsy: Recurrent, unprovoked seizures Etiologies: Unknown cause, metabolic disorders, CNS infection, tumor, and noncompliance with epilepsy medications
Focal Seizures
Without dyscognitive features (aware): May have sensory changes, autonomic symptoms, speech arrest, aura, or psychic symptoms With dyscognitive features (unaware): Most common seizure, with simple partial seizure followed by loss of awareness and automatisms, often beginning with an aura
Generalized Seizures
Typical absence seizures: Sudden loss of consciousness (5-30 seconds), mild clonic/tonic movements, several times per day Atypical absence seizures: Longer loss of consciousness, obvious motor symptoms Generalized tonic-clonic seizures: Abrupt start with outcry, loss of consciousness/falling, respiratory arrest, tonic and clonic movements, urinary incontinence, 2-5 minutes, postictal state
Status Epilepticus
A prolonged seizure (longer than 5 minutes) or a situation when a person suffers two or more convulsive seizures without regaining full consciousness Requires aggressive treatment, a medical emergency
Seizure Diagnosis and Management
Diagnostic tests: EEG/24 hours, CT head, LP (if CT or MRI did not show anything), CBC, BMP, UA (drug screen), and elevated prolactin Management: Supportive care: Airway, left side laying, do not force anything in mouth IV with normal saline Benzodiazepines (Ativan, Diazepam, Midazolam) as first-line treatment
Cellulitis
Infection of the dermis and subcutaneous tissue Caused by Gram-positive cocci (Staphylococcus aureus, Streptococcus) and Gram-negative bacteria (E. coli) Risk factors: Trauma, underlying skin lesion, diabetes, pedal edema, venous/lymphatic compromise, IV drug use
Cellulitis Results
Tenderness, pain, swelling, erythema, warmth Rapid increase in intensity and spread Fever, chills, malaise, possible sepsis Erythema with indistinct margins, warmth, and tenderness Enlargement and tenderness of regional lymph nodes Red streaks from the site (lymphangitis) Rule out DVT and necrotizing fasciitis
Cellulitis Treatment
Antibiotics: Penicillin, Cephalexin, Dicloxacillin, or Erythromycin/ Clindamycin for penicillin allergy Inpatient antibiotics: Nafcillin, Cefazolin, Vancomycin for MRSA suspicion Immobilization, elevation of the limb, moist heat Low-dose, long-term penicillin for recurrent cellulitis
Herpes Zoster (Shingles)
Reactivation of latent varicella-zoster virus, characterized by unilateral pain present 48 hours before rash Affects individuals older than 50 or with impaired immune systems (lymphoma, fatigue) Can lead to post-herpetic neuralgia for up to 1 month
Herpes Zoster Results and Diagnostics
Prodromal pain symptoms (sharp, burning, itching) in the affected spot Malaise, low-grade fever, headache, allodynia, lymphadenopathy Grouped vesicles on an erythematous, tender base along a nerve group ECG during prodromal phase to rule out cardiac illness VZV antigen detection, positive Tzanck test, and viral culture
Herpes Zoster Management
Consult ophthalmology for Herpes Zoster on the tip of the nose Antiviral therapy (Acyclovir) for 50-50-50 rule: 50 hours or less since onset, 50 years or older, more than 50 lesions Pain control with opioids, moist dressing, Hydroxyzine for pruritus Post-herpetic neuralgia pain: Lidocaine patch, Pregabalin
Skin Cancer
Basal Cell Carcinoma
Most common type of skin cancer Affects fair-skinned people, slowly grows 1-2 cm over years, limited capacity to metastasize Associated with sun exposure before age 14, rare in brown/black people, occurs on the face and neck
Squamous Cell Carcinoma
Wart-like appearance, from actinic/solar keratosis Can metastasize, especially on the lip, oral cavity, tongue, and genitals Result of exogenous carcinogens
Skin Cancer: BCC and SCC
BCC and SCC Results and Diagnostics
BCC (Basal Cell Carcinoma): Nodule or ulcerative tumor: Small, pearly, waxy. Translucent borders, elevated and shiny fine telangiectasis.
Superficial BCC: Erythematous scaly macule with threadlike border.
SCC (Squamous Cell Carcinoma):
Firm, skin to red-colored nodule on damaged skin. Central ulceration. Scaling and crusting.
Commonly occurs on the head/neck.
Biopsy:
Shaved biopsy (for raised lesions). Punch biopsy (small distinct bordered lesion).
Incisional biopsy (large lesion).
Treatment:
Curettage and electrodesiccation in three cycles for BCC lesions smaller than 1cm (gold standard).
Skin Cancer: BCC and SCC Management
Consult a dermatologist. Treatment options: Cryosurgery.
Level 5: Invasion subcutaneous fat.
Breslow Staging:
Thin: Less than 0.75mm depth. Intermediate: 0.76 - 3.99mm depth. Thick: Greater than 4mm depth.
Melanoma Management
Consult a dermatologist. Follow-up every 3-6 months. Based on stage: Less than 1mm: Wide excision 1mm. No lymph node dissection. 1-4mm thick: Wide excision 2mm. Nodal biopsy recommended. Lymphatic mapping. Greater than 4mm thick: Wide excision more than 4mm. Adjuvant therapy: Hematology/oncology. Alpha-interferon.
Kinds of Wounds
Acute Wounds
Acute surgical: Clean/contaminated. Traumatic wound: Clean/contaminated.
Chronic Wounds
Arterial: Ischemia from arterial occlusive illness. Venous: Venous return disorder. Diabetic: From hyperglycemia and peripheral neuropathy. Pressure: Prolonged pressure.
Factors that Delay Wound Healing
Pressure. Reduced tissue perfusion/oxygenation. Incontinence. Infection. Diabetes mellitus. Poor nutrition. Steroids. Immunosuppression. Aging.
Wound Results and Specifics
Pain: Arterial: Claudication. Venous: Lower extremities heavy and sore.
Neuropathy: Numbness, tingling. Arterial, venous, diabetic: Poor healing.
Wound Depth and Levels
Superficial. Partial thickness: Through epidermis, partially into dermis. Full thickness: Through epidermis and dermis and some subcutaneous layer. Muscle/bone may be involved. Undermining and tunneling.
Wound Colors
Red: Healthy. Yellow: Debridement/cleaning needed. Black: Necrotic.
Results of Arterial and Diabetic Ulcers
On toes and below ankles (arterial). Plantar surfaces of feet (diabetic). Diminished pulse. Shiny, cool leg skin. No leg hair. Thick toe nails. Deep ulcer with smooth wound margins, small amount of drainage/ necrosis.
Results of Venous Ulcers
Lower legs, above ankle. Varicoses present. Edema of leg. Warm leg. Superficial, granulating ulcer with irregular margins, with heavy drainage.
Results of Pressure Ulcers
On bony prominences. Stage 1: Skin intact, but skin non-blanchable. Stage 2: Partial thickness loss. Stage 3: Full thickness loss, deep crater-like. Stage 4: Full thickness and extensive destruction with tissue necrosis.
Diminished Arterial and Venous Flow Diagnostics
Doppler, reduced PVR waveforms. Digital plethysmography: Systolic toe pressure. Normal is 80-90%. Transcutaneous oxygen measurements: Higher than 30, wound will heal. Lower than 20, will not heal.
