Codeine

30/09/2009

 

 

Classification

 

  • Allergy

  • Cold

  • Cough

  • Opioid Analgesic

 

Indications:

 

  • management of mild to moderate pain

  • Antitussive in small doses

  • Off label use = management of diarrhea

 

Action

 

  • binds opiate receptors in the CNS

  • Alters perception and response to pain stimuli

  • general CNS depressant

  • depresses cough reflex

  • Decreases GI motility

 

Contraindications/Cautions:

 

  • Hypersensitivity

  • Head Trauma

  • Increased Intracranial pressure

  • severe renal hepatic or renal pulmonary disease

  • hypothryroidism

  • adrenal insufficiency

  • alcoholism

  • Geri or debilitated: dose reduction, increased susceptibility to CNS depression and constipation

  • Geri: Prostatic Hyperplasia

  • OB: use during labor, respiratory depression may occur in newborn

 

Adverse Rxns/Side Affects

 CNS

  • confusion

  • sedation

  • dysphoria

  • euphoria

  • floating feeling

  • hallucinations

  • headache

  • unusual dreams

EENTeyes, ears, nose and throat

  • blurred vision

  • diplopia

  • miosis (constriction of the pupil of the eye.)

 

Respiratory

  • Respiratory depression

CV

  • hypotension

  • bradycardia

GI

  • constipation

  • nausea

  • vomiting

 GU

  • urinary retention

 Derm

  • Flushing

  • Diaphoresis

 Misc

  • Physical Dependence

  • psychological dependence

  • tolerance

 

Interactions

 

  • MAO inhibitors (reduce initial dose to 25% of usual dose)

 

Additive CNS depression with:

  • alcoholics
  • antidepressants
  • antihistamines

  • sedative/hypnotics

 

Antagonistic effects (partial)

  • buprenorphine

  • butorphanol

  • nalbuphine

  • pentazocine

  • may ppt withdrawal in physically dependent patients

 

Nalbuphine and pentazocine may decrease analgesia

 

Dosage/Route

  • IV

  • IM

  • PO

 

Assessment

 

  • assess BP Pulse, Resp before and during administration

  • If resp is <10/min assess lvl of sedation

  • Initial drowsiness may diminish with subsequent use

  • Assess bowel function: increase fluid intake, bulk and laxatives

  • Simulant laxatives should be administered routinely if opioid use exceeds 2-3 days

 

Pain:

  • assess pain type, location and intensity before and 1hr after administration (peak)

  • increases of 25-50% should be administered until there is either a 50% decrease in numerical pain scale reported or pt reports satisfactory relief

  • An equianalgesic chart should be used when changing from one analgesic to another

 

Antidote: Narcan

 

Patient Teaching:

 

  • may cause drowsiness caution against driving or other activities that require high alertness

  • advise pt to change position slowly to avoid orthstatic hypotension

  • caution pt to turn, cough, breath deeply every 2hr to avoid atelectasis

  • Good oral hygiene, mouth rinse and sugarless gum may decrease fry mouth

Hazard Vallerand, April,  and Hopfer Deglin , Judith. 2007. Davis` Drug Guide for Nurses. 11th ed. F. A Davis Company, USA.


Dysarthria

29/09/2009

Dysarthria is a motor speech disorder. 

This results in impaired articulatory ability, speech that is slowed, slurred or distorted.

Etiology:

Difficulty in forming words or speaking them because of weakness of muscles used in speaking or because of disruption in the neuromotor stimulus patterns required for accuracy and velocity of speech, such as neurological injury.

Alcoholic cerebellar degeneration

This disorder commonly causes chronic, progressive dysarthria along with ataxia, diplopia, ophthalmoplegia, hypotension, and altered mental status.

Amyotrophic lateral sclerosis

Dysarthria occurs when this disorder affects the bulbar nuclei; it may worsen as the  disease progresses. Other signs and symptoms include dysphagia; difficulty breathing; muscle atrophy and weakness, especially of the hands and feet; fasciculations; spasticity; hyperactive DTRs in the legs; and occasionally excessive drooling. Progressive bulbar palsy may cause crying spells or inappropriate laughter.

Basilar artery insufficiency

This disorder causes random, brief episodes of bilateral brain stem dysfunction, resulting in dysarthria. Accompanying it are diplopia, vertigo, facial numbness, ataxia, paresis, and visual field loss, all of which can last from minutes to hours.

Botulism

The hallmark of this disorder is acute cranial nerve dysfunction that causes dysarthria, dysphagia, diplopia, and ptosis. Early findings include dry mouth, sore throat, weakness, vomiting, and diarrhea. Later, descending weakness or paralysis of muscles in the extremities and trunk causes hyporeflexia and dyspnea.

Multiple sclerosis

When demyelination affects the brain stem and cerebellum, the patient displays dysarthria accompanied by nystagmus, blurred or double vision, dysphagia, ataxia, and intention tremor. Exacerbations and remissions of these signs and symptoms are common. Other findings include paresthesia, spasticity, intention tremor, hyperreflexia, muscle weakness or paralysis, constipation, emotional lability, and urinary frequency, urgency, and incontinence.

Myasthenia gravis

This neuromuscular disorder causes dysarthria associated with a nasal voice tone. Typically, the dysarthria worsens during the day and may temporarily improve with short rest periods. Other findings include dysphagia, drooling, facial weakness, diplopia, ptosis, dyspnea, and muscle weakness.

Olivopontocerebellar degeneration

Dysarthria, a cardinal sign of this disorder, accompanies cerebellar ataxia and spasticity.

Parkinson’s disease

This disorder produces dysarthria and a monotone voice. It also produces muscle rigidity, bradykinesia, an involuntary tremor that usually begins in the fingers, difficulty walking, muscle weakness, and stooped posture. Other findings include masklike facies, dysphagia and, occasionally, drooling.

Shy-Drager syndrome

Marked by chronic orthostatic hypotension, this syndrome eventually causes dysarthria as well as cerebellar ataxia, bradykinesia, masklike facies, dementia, impotence and, possibly, stooped posture and incontinence.

Stroke (brain stem)

This type of stroke is characterized by bulbar palsy, resulting in the triad of dysarthria, dysphonia, and dysphagia. The dysarthria is most severe at the onset of the stroke; it may lessen or disappear with rehabilitation and training. Other findings include facial weakness, diplopia, hemiparesis, spasticity, drooling, dyspnea, and decreased LOC.

Stroke (cerebral)

A massive bilateral stroke causes pseudobulbar palsy. Bilateral weakness produces dysarthria that’s most severe at the stroke’s onset. This sign is accompanied by dysphagia, drooling, dysphonia, bilateral hemianopsia, and aphasia. Sensory loss, spasticity, and hyperreflexia may also occur.

Drugs

Dysarthria can occur when anticonvulsant dosage is excessive. Ingestion of large doses of barbiturates may also cause dysarthria.

Manganese poisoning

Chronic manganese poisoning causes progressive dysarthria accompanied by weakness, fatigue, confusion, hallucinations, drooling, hand tremors, limb stiffness, spasticity, gross rhythmic movements of the trunk and head, and a propulsive gait.

Mercury poisoning

Chronic mercury poisoning causes progressive dysarthria accompanied by weakness, fatigue, depression, lethargy, irritability, confusion, ataxia, and tremors.

Assessment:

If the patient displays dysarthria:

  • query associated difficulty swallowing
  • determine respiratory rate and depth.
  • measure vital lung capacity with a Wright respirometer if available.
  • assess blood pressure and heart rate
  • Tachycardia, slightly increased blood pressure, and shortness of breath are usually early signs of respiratory muscle weakness.

Management:

  • Ensure a patent airway.
  • Place the patient in Fowler’s position
  • Suction him if necessary.
  • Administer oxygen
  • Keep emergency resuscitation equipment nearby.
  • Anticipate intubation and mechanical ventilation in progressive respiratory muscle weakness.
  • Withhold oral fluids in the patient with associated dysphagia.

Follow-up:

  • If dysarthria isn’t accompanied by respiratory muscle weakness and dysphagia, continue to assess for other neurologic deficits.
  • Compare muscle strength and tone in the limbs, and evaluate tactile sensation.
  • Query patient about numbness or tingling.
  • Test deep tendon reflexes (DTRs), and note gait ataxia.

  • Assess cerebellar function by observing rapid alternating movement, which should be smooth and coordinated.
  • Test visual fields and ask about diplopia.
  • Check for signs of facial weakness such as ptosis.
  • Determine level of consciousness (LOC) and mental status (MMSE).

Springhouse. 2006. Professional Guide to Signs & Symptoms, Fifth Edition. Lippincott Williams & Wilkins.

Retrieved September, 29, 2009 from http://images.google.ca/imgres?imgurl=http://www.wrongdiagnosis.com/bookimages/8/2554.1.png&imgrefurl=http://www.wrongdiagnosis.com/symptoms/speech_symptoms/book-causes-8a.htm&usg=__VqUsn8CJgrQKcAtlSE3GQqqyAUQ=&h=654&w=497&sz=33&hl=en&start=2&um=1&tbnid=PpApdiKJHhMqfM:&tbnh=138&tbnw=105&prev=/images%3Fq%3Ddefine:Dysarthria%26hl%3Den%26sa%3DN%26um%3D1


Types of Wound Exudate

28/09/2009

Types of exudate:

 

An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation.

Exudate is derived from exude, “to ooze

Its composition varies but generally includes water and the dissolved solutes of the main circulatory fluid.

 

 

  1. Serous exudate

  • Contains: serum – no cells or clotting factors

  • note: plasma differs from serum in that it contains no cells but contains clotting factors

  • Consistency: watery

  • Colour: clear

  • Indicative of mild, acute inflammation

 

2. Purlent/suppurative exudate

  • Contains: WBC, bacteria, fluid, proteins, fibrinogen and necrotic cellular debris

  • Consistency: thick fluid

  • Colour: white

  • Indicative of severe infection and injury

 3. Hemoragic exudate

  • Contains: whole blood

  • Consistency: fluid

  • Colour: blood red

  • Indicative of capilliary rupture

 4. Fibrinous exudate

  • Contains: High concentrations of Fibrinogen and Fibrin

  • Consistency: Thick sticky meshwork

  • Colour: yellowish, clear

  • Indicative of severe injury

  • Fibrinous inflammation is often difficult to resolve due to the fact that blood vessels grow into the exudate and fill the space that was occupied by fibrin. Often, large amounts of antibiotics are necessary for resolution.

 

.

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia


Depression

26/09/2009

Definition:

A change in mood which lasts at least 2 weeks and includes sadness, negativity, loss of interest, pleasure and /or decline in functioning.

Duration:

At least 6 weeks, but can last several months to years, especially if not treated.

Thinking:

May be indecisive and thoughts highlight failures and a sense of hopeless.

Mental Status Testing:

Capable of giving correct answers, however often may state “I don’t know”

Memory:

Generally intact, thought may be selective. Highlights negativity.

Sleep wake cycle

Disturbed, usually early morning awakening.

Hallucination and delusions:

Can be present in severe depression. Themes of guilt and self-loathing.

Diagnosis

May deny being depressed but often exhibit anxiety. Others may notice symptoms first. Increased complaints of physical illness. Social withdrawal is common.

Care approaches:

Identify the symptoms of depression early. Help person to follow treatment offer support.

Prognosis:

Treatable and reversible condition.

Treatment:

antidepressants, ECT, interpersonal therapy, behavior therapy. Assist individual to improve confidence and self esteem through conversation and physical activity.

Forman, MD and Zane, D. 1996. Nursing strategies for acute confusion in elders. American Journal of Nursing. 96 (4) 44-51.

Lipowski, Z. 1989. Delirium in the elderly Patient. The New England Journal of Medicine. 320 (9) 578-582.


Types of Dementia

25/09/2009

Alzheimer’s disease – Alzheimer’s dementia is the most common type of dementia, and is caused by a loss of brain cells. It is at least partly a hereditary disease, in that it tends to run in families. (Just because a relative has Alzheimer disease, however, does not mean that another family member will have the disease.) In this disease, cells in the areas of the brain that control memory and mental functions are destroyed by abnormal protein deposits in the brain. People with Alzheimer disease also have lower-than-normal levels of brain chemicals called neurotransmitters that control important brain functions. Alzheimer disease is not reversible, and there is no known cure. There are, however, medications that can slow its progress.

Vascular dementias, including multi-infarct dementia – Vascular dementias is the next most common type of dementia, and is caused by poor circulation of blood to the brain. In multi-infarct dementia, lots of tiny strokes (or infarcts) occur which cut off the blood supply to part of the brain. The progression of vascular dementia can happen in recognised steps. With this type of dementia, good control of blood pressure, good diabetic control and avoiding cigarettes may help to slow the progress.

Parkinson disease – People with this disease typically have limb stiffness (which causes them to shuffle when they walk), speech problems, and tremor (shaking at rest). Dementia may develop late in the disease, but not everyone with Parkinson disease has dementia. Reasoning, memory, speech, and judgment are most likely to be affected.

Lewy body dementia – This is caused by abnormal microscopic deposits of protein in nerve cells, called Lewy bodies, which destroy the cells over time. These deposits can cause symptoms typical of Parkinson disease, such as tremor and muscle rigidity, as well as dementia similar to that of Alzheimer disease. Lewy body dementia is more likely, however, to affect thinking, attention, and concentration than memory and language. Like Alzheimer disease, Lewy body dementia is not reversible and has no known cure. The drugs used to treat Alzheimer disease also benefit some people with Lewy body disease.

Alcohol-related dementia – Brain damage can be caused by drinking too much alcohol. It is important that people with this type of dementia give up drinking alcohol completely to stop the disease progressing.

Pick disease (frontotemporal dementia) – Pick disease is another rare disorder that damages cells in the front part of the brain. Behavior and personality changes usually precede memory loss and language problems.

 

What types of Dementia are there? Retrieved September 25, 2009 from http://neurology.health-cares.net/dementia-types.php


Deliriuim

24/09/2009

Definition:

An acute or sudden onset of mental confusion as a result of a medical, social and/or environmental condition.

Thought Process:

Fluctuates between rational state and disorganized, distorted thinking with incoherent speech.

Memory Impairment:

Recent and immediate memory impaired

Effects on Sleep-wake Cycle

Disturbed. Sleep-wake cycle is reversed (up in night, very sleepy and sometimes non-responsive during the day)

Hallucinations and delusions:

 Often of a frightening or paranoid nature

Diagnosis:

Diagnosis based on rapid onset of fluctuating symptoms. Can be mistaken for progression of the dementia.

Care Approaches:

Early recognition is key. Keep person safe, find cause of the delirium and treat as quickly as possible.

Prognosis:

Treatable and reversible with early diagnosis but can lead to permanent disability or death.

Treatment:

Treat underlying cause. Monitor response. Be alert for relapse, occurs in 90% of causes

 

Forman, MD and Zane, D. 1996. Nursing strategies for acute confusion in elders. American Journal of Nursing. 96 (4) 44-51.

Lipowski, Z. 1989. Delirium in the elderly Patient. The New England Journal of Medicine. 320 (9) 578-582.


Bell’s Palsy

23/09/2009
  • Temporary Facial paralysis
  • Mild muscle weakness

Etiology

Bell’s Palsy results from nerve damage or trauma to one of the two facial nerves. There is one facial nerve on either side of the face.

Bell’s Palsy occurs when the nerve that controls the facial muscles is swollen, inflamed, or compressed, resulting in facial weakness or paralysis

Facial Nerve

  • Cranial nerve VII: The facial nerve emerges from the brainstem between the pons and the medulla, and controls the muscles of facial expression, and taste to the anterior two-thirds of the tongue.

Facial Nerve Functions:

  •  control eye blinking and closing
  • facial expressions such as smiling and frowning
  • carries nerve impulses to the lacrimal or tear glands, and the saliva glands
  • Innervates the muscles of a small bone in the middle of the ear called the stapes. The facial nerve also transmits taste sensations from the tongue.