“What is an Incident Report” plus 5 more nursing article(s): NursingCrib.com Updates

What is an Incident Report
Pediatric Nephrotic Syndrome
Chelation Therapy
Difference between a Cow’s Milk and Human Breast Milk
Corynbacterium Diptheriae
Clostridium Perfringens

Posted: 16 Dec 2010 09:03 PM PST

Definition

Despite the most careful precaution of medical personnel, medico-legal accidents still occur. In all cases of accidents nurses caring for the client during the time of incident and those who saw or heard the unusual event should write an incident report. The nurse in charge of the department should also write an incident report in cases of accident.

An incident report is a form that filled up in order to record the details of accidents, patient injury and other unusual events that occur in a health care facility such as a hospital or nursing home. It is also called an accident report which documents the exact details of the accident or unusual event while the information is still fresh in the minds of those who witness the event.

Purpose of an Incident Report

People often regard an incident report as a black mark against the nursing staff who wrote it. This should not be the case because an informed consent is a legal document of an incident that took place. The purposes of an incident report are the following:

To document the exact detail of an accident or unusual incident that occurred in a health-care institution.
To be used in the future when dealing with liability issues stemming from the incident.
To protect the nursing staff against unjust accusation.
To protect and safeguard the client in case of negligence on the part of the nurse.
Helps in the evaluation of nursing care to ensure safe care to all patients.

Incident Report

Written at the first opportunity after the incident so that the details are not blurry or forgotten.
Written with a pen (ink) not pencil. Information written using a pencil can be erased.
Details should be complete and accurate. The patient should be identified with the following details:

Full name
Hospital bed number
Hospital ID
Patients diagnosis
Patient's condition before and after the incident

Other details included are:

Details of ward or clinical area
Date, time and place of incident
Details of equipments used including the serial number or asset tag identification (if appropriate)

Written as statement of facts without interpretation or opinion. Descriptive adjectives should not be used.

For example instead of writing:

"Mr. Dimaano would not listen when I told him to stay in bed. He is very difficult to care for. It is his fault why he fell on the floor."

You should write:

"I heard a loud crash, and immediately went to the ward. I found Mr. Dimaano on the floor."

Events should be written in sequence that they occurred.
Proper technical terms should be used. For example instead of using the word bottle specify that it is a urinal.
Identifies the witnesses.
Identifies the medications given before the incident (if applicable)
Identifies the equipment that is involved or used.
Signed legibly with the correct designation.

image from ppo.tamuk.edu

Pediatric Nephrotic Syndrome

Posted: 16 Dec 2010 08:34 PM PST

Pediatric Nephrotic Syndrome

Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, and edema.
Pediatric nephrotic syndrome are usually the primary type.
Approximately 85% to 95% of primary cases in preadolescents are minimal change nephrotic syndrome and are associated with minimal histologic changes in the glomeruli.
Nephrotic syndrome annually inflicts about 16 children per 100,000 younger than age 16 in the United States.
It is slightly more common in males than females in younger children, but this disappears in teenagers and adults.
Mean age of onset is 2 and a half years.

Pathophysiology:

Underlying defect is thought to be caused by the loss of charge selectivity of the glomerular basement membrane, which permits negatively charged proteins, primarily albumin, to pass easily through the capillary walls into the urine.
Excessive urinary loss of protein and catabolization by the kidney of circulating albumin leads to a decrease in serum protein.
The colloidal osmotic pressure that holds water in the vascular compartments is reduced because of the decrease in the amount of serum albumin. This allows fluid to flow from the capillaries into the interstitial spaces, thus producing edema.
The shift of fluid from the plasma to the interstitial spaces reduces the vascular fluid volume, which in turn stimulates the renin-angiotensin system and the secretion of the the antidiuretic hormone and aldosterone.
Tubular resorption of sodium and water is increased to increase intravascular volume.
The loss of proteins, particularly immunoglobulins, predisposes the child to infection.

Clinical Manifestations:

Edema

Periorbital edema usually becomes apparent first
Dependent edema in the hands, ankles, feet, genitalia
Ascites and pleural effusions
Striae due to overstretching

Profound weight gain
Decreased urine output
Pallor, irritability, lethargy, fatigue
GI disturbances such as vomiting, diarrhea and anorexia

Diagnostic Evaluation:

Urinalysis, usually with protein of 2+ or greater
24-hour urine protein, frequently greater than 2 g/m2 per day
Total protein and albumin reduced
Cholesterol, greater than 200 mg/dL

Complications:

Peritonitis
Septicemia
Cellulitis
Thrombosis
Acute renal failure

Management:

Steroid therapy
Immunosuppressants:

Cyclophosphamide
Cyclosporin A
Tacrolimus

IV Albumin 25%

Nursing Management:

Relieve excess fluid by administering steroids or alternative drugs as prescribed.
Offer foods high in potassium, low in sodium, fat and sugar.
Encourage activity as tolerated.
Restrict fluids as ordered. Strictly monitor intake and output.
Weigh patient daily.
Provide meticulous skin care to the edematous parts of the body.
Give emotional support to the child and his parents.
Help child adjust to body image changes by explaining changes ahead of time.

Photo credits: www.medicaldude.com

Chelation Therapy

Posted: 16 Dec 2010 08:17 PM PST

Definition

Chelation therapy is the administration of chelating agents to remove heavy metals in the body. It is very helpful in cases of poisoning and the most common forms of metal intoxication such as lead, mercury and arsenic poisoning. Chelating agents combine with metals and allow them to be excreted from the body.

Indications of chelating therapy:

Mercury poisoning
Iron poisoning
Arsenic poisoning
Lead poisoning
Uranium
Plutonium and
Other forms of heavy metals

Mechanisms of Action

The human body is unable to break down heavy metals. When these elements build up and reach toxic levels in the body it can interfere with the normal functioning of a person. Chelating agents lower the blood levels of metals (e.g. lead, iron, etc.). This is made possible by the attachment of heavy metal molecules to the administered chelating agents. The heavy metal attached to the chelating drugs is then removed in the body through urination.

Common Chelating Agents

Chelating Agent	Indication for use
Dimercaprol (BAL)	Acute arsenic poisoning Acute mercury poisoning Lead poisoning (with another chelating drug, EDTA)
Edetate calcium disodium or Ethylenediamine tetraacetic acid (CaEDTA or EDTA)	Lead poisoning
Deferoxamine	Acute Iron poisoning Iron overload
Dimercaptosuccinic Acid (DMSA)	Lead poisoning Arsenic poisoning Mercury poisoning
Dimercapto-propane sulfonate (DMPS)	Severe acute arsenic poisoning Severe acute mercury poisoning
Penicillamine	Copper toxicity (mainly used) Adjunct to the therapy in: Gold poisoning Arsenic poisoning Lead poisoning
Succimer (Chemet)	Lead poisoning in pediatric patients with blood lead levels above 45 microgram per deciliter

Side Effects

Burnings sensation at the site of injection or delivery into the vein (common)
Fever
Headache
Nausea
Stomach upset
Vomiting
Flu-like symptoms
Convulsions
Bone marrow depression
Hypotension
Cardiac arrhythmia
Respiratory arrest
Hypocalcemia
Kidney failure (rare)
Death (rare)

Contraindications

Hypersensitivity or known allergy to the drugs

Nursing Implications

Obtain serum levels of heavy metals (e.g. lead, iron) before the initiation of therapy and again at the termination of the therapy.
Instruct the parents and child about the need to comply with the full course of medication regimen to achieve desired outcome and effectiveness.
For EDTA: Monitor serum calcium levels as EDTA removes calcium in the body.
For EDTA: Injections of EDTA must be given intramuscularly into a large muscle mass. The medication can be combined with 0.5 ml of PROCAINE as the injection of this drug is very painful.
Measure intake and output to ensure that the kidney is adequately functioning. (If kidney function is not adequate EDTA may lead to nephrotoxicity or kidney damage)
Assess the following:

BUN
Serum creatinine
Protein in urine

image from ncdaustralia.com.au

Difference between a Cow’s Milk and Human Breast Milk

Posted: 16 Dec 2010 08:03 PM PST

Newborns and infants need sufficient nutrition to be sued for their growth and development. To meet energy needs, prevent the use of body stores and to provide for growth the infant must consume adequate calories. Nutrients needed by neonates such as carbohydrates, proteins, and fat are contained in breast or formula milk. Full-term neonates digest simple carbohydrates and protein well. Fats are less digested because of the lack of pancreatic enzyme in the newborn. Aside from nutrients and calories, newborns also need larger amount of fluid. Water is unnecessary to be given as breast milk or formula already supplies the infant's fluids needs.

Daily Calorie and Fluid Needs of the Newborn

(Source: Saunders' Foundations of Maternal-Newborn Nursing by Murray and McKinney)

Calories

110-120 kcal/kg (50-55 kcal/lb)

Fluid

40 to 60 ml/kg (18-27 ml/lb) for the first two days of life
100 to 150 ml/kg (45-68 ml/lb) by the end of the first week

Breast Milk

Breast milk offers many advantages compared to that of formula. Not only that nutrients are proportioned appropriately in breast milk to meet the neonate's changing needs but it also provides protection against infection. Composition of breast milk changes in three phases which are the following:

Colostrum – secreted during the first week of lactation. It is a yellowish and thick substance. This type of breast milk contains higher protein, fat-soluble vitamins and minerals than the mature milk. However, it contains lower calories, fat and lactose. It is also rich in immunoglobulin that helps in the protection of the GI tract from infection.
Transitional Milk – contains lesser immunoglobulin and proteins. Lactose, fat and calories are increased in this type of breast milk.
Mature milk – replaces transitional milk after 2 weeks of lactation. Contains 20 kcal/oz and nutrients essential for infant's growth and development.

Cow's Milk

Modified cow's milk is the source of most commercial formulas. It is specifically formulated for infants. The protein component is reduced to decrease the renal solute load. Vegetable fat replaces the saturated fat of an unmodified cow's milk. To simulate the contents of breast milk, vitamins and other nutrients are added to the preparation.

Content	Breast Milk	Cow's Milk
Protein: Casein Whey	High ratio of whey to casein (that makes it more easily digested)	Contains high casein (not easily digested)
Carbohydrate: Lactose	6.8 g/dl	4.9 g/dl
Vitamin C	43 mg	11 mg
Iron	0.5 mg	0.5 mg (High casein and low Vitamin C concentration of cow's milk level interferes with iron absorption.)
Vitamin D	22 iu	14 iu

Corynbacterium Diptheriae

Posted: 16 Dec 2010 08:01 PM PST

DESCRIPTION

A Gram (+), aerobic, nonsporeforming, club-shaped pleomorphic rods in palisade or Chinese letter character formation.

Nonmotile, facultatively anaerobic, catalase (+), and ferment carbohydrates
Inhabits the skin, URT, GIT, and urogenital tract of man
Grow slowly on enriched media (e.g. cysteine-tellurite agar, serum tellurite agar, Loeffler's medium and McLeod's chocolate tellurite agar.
On blood agar with potassium tellurite, colonies are black. The black color is due to the precipitation of tellurious ions that diffused into the cell wall.
Resistant to light, dessication, and freezing.
Easily killed by boiling for one minute or when kept in a temperature of 58^oC for 10 minutes
Destroyed by antiseptics, chemical disinfectants.
Causes diphtheria

DIPHTHERIA

An acute infectious disease of the URT (nose, tonsils, larynx, pharynx, mucous membran es and the skin) which usually begins as a pharyngitis associated with dull red inflammatory zone of "pseudomembrane formation" and lymphadenopathy.
Formation of a false membrane is the result of the absorption of the affected area of a potent diphtheria exotoxin which become necrotic, and embedded in the fibrin, red blood cells and white blood cells.
The toxin can cause remote damages to the heart, liver, and kidneys.
Incubation period is 2 to 6 days.
It is common among children.

RISK FACTORS/CAUSES

Direct contact with a patient or carrier through sneezing or by droplet infection
Indirectly through use of contaminated fomites of the patient.

SIGNS AND SYMPTOMS

thick mucopurulent nasal discharges
fever
cough
hoarseness of the voice
sore throat
swelling of the lymphnodes

Although Corynecbacterium Diphtheriae may infect the skin, it rarely invades the bloodstream and never actively invades deep tissue.

TYPES AND CATEGORIES

Four Clinical Forms of Diphtheria

Faucial. Pharyngeal – The membrane spreads rapidly from the tonsils across the soft palate to the uvula and over the pharyngeal wall into the naso-pharynx.
Laryngeal – membrane formation may easily cause suffocation.
Tonsillar– membrane is confined to the tonsils, where absorption of the toxin is moderate.
Nasal – membrane formation is rarely associated with severe disease because toxin is poorly absorbed by the lining of the nose.

PREVENTION

Isolation of sick persons
Detection and treatment of healthy carriers with antibiotics for seven days.
Active immunization against symptomatic diphtheria with diphtheria toxoid during childhood and booster immunization every 10 years throughout life.

MANAGEMENT

Early use of diphtheria antitoxin for the specific neutralization of exotoxin.
Antibiotic therapy with penicillin or erythromycin.
Bed rest and isolation to prevent secondary spread.
Maintenance of an open airway in patients with respiratory diphtheria.

Photo credits: www.waterscan.rs

CORYNEBACTERIUM DIPHTHERIAE

DESCRIPTION

A Gram (+), aerobic, nonsporeforming, club-shaped pleomorphic rods in palisade or Chinese letter character formation.

· Nonmotile, facultatively anaerobic, catalase (+), and ferment carbohydrates

· Inhabits the skin, URT, GIT, and urogenital tract of man

· Grow slowly on enriched media (e.g. cysteine-tellurite agar, serum tellurite agar, Loeffler's medium and McLeod's chocolate tellurite agar.

· On blood agar with potassium tellurite, colonies are black. The black color is due to the precipitation of tellurious ions that diffused into the cell wall.

· Resistant to light, dessication, and freezing.

· Easily killed by boiling for one minute or when kept in a temperature of 58^oC for 10 minutes

· Destroyed by antiseptics, chemical disinfectants.

· Causes diphtheria

DIPHTHERIA

· An acute infectious disease of the URT (nose, tonsils, larynx, pharynx, mucous membranes and the skin) which usually begins as a pharyngitis associated with dull red inflammatory zone of "pseudomembrane formation" and lymphadenopathy.

· Formation of a false membrane is the result of the absorption of the affected area of a potent diphtheria exotoxin which become necrotic, and embedded in the fibrin, red blood cells and white blood cells.

· The toxin can cause remote damages to the heart, liver, and kidneys.

· Incubation period is 2 to 6 days.

· It is common among children.

RISK FACTORS/CAUSES

· Direct contact with a patient or carrier through sneezing or by droplet infection

· Indirectly through use of contaminated fomites of the patient.

SIGNS AND SYMPTOMS

Typical symptoms include thick mucopurulent nasal discharges, fever, cough, hoarseness of the voice, sore throat and swelling of the lymphnodes. Although Corynecbacterium Diphtheriae may infect the skin, it rarely invades the bloodstream and never actively invades deep tissue.

TYPES AND CATEGORIES

Four Clinical Forms of Diphtheria

1. FAUCIAL/PHARYNGEAL – The membrane spreads rapidly from the tonsils across the soft palate to the uvula and over the pharyngeal wall into the naso-pharynx.

2. LARYNGEAL – membrane formation may easily cause suffocation.

3. TONSILLAR – membrane is confined to the tonsils, where absorption of the toxin is moderate.

4. NASAL – membrane formation is rarely associated with severe disease because toxin is poorly absorbed by the lining of the nose.

PREVENTION

· Isolation of sick persons

· Detection and treatment of healthy carriers with antibiotics for seven days.

· Active immunization against symptomatic diphtheria with diphtheria toxoid during childhood and booster immunization every 10 years throughout life.

MANAGEMENT

· Early use of diphtheria antitoxin for the specific neutralization of exotoxin.

· Antibiotic therapy with penicillin or erythromycin.

· Bed rest and isolation to prevent secondary spread.

· Maintenance of an open airway in patients with respiratory diphtheria.

Clostridium Perfringens

Posted: 16 Dec 2010 07:45 PM PST

CLOSTRIDIUM PERFRINGENS

DESCRIPTION

Large, rectangular, non-motile, sporeforming, gram (+), capsulated, arranged singly or in pairs
Grows well in cooked meat and milk media under anaerobic conditions
Ferments glucose, fructose, and lactose in milk medium with production of large amounts of gas – hence the name "gas bacillus" giving a characteristic "stormy fermentation of milk" in this medium
Common inhabitants of the soil, street dust and feces or manure of herbivorous animals
Causes gas gangrene

GAS GANGRENE

This is brought about when the bacilli invade the tissues of the body through deep punctured wounds due to vehicular accidents, gunshot wounds, compound fracture of postpartum uterus.
Inside the tissues, the organism grows especially in the muscle fibers with such vigor that the pressure of accumulated gas tears the tissues apart.
The infection spread in 1 to 3 days to produce crepitation (filling of air inside the tissue).

RISK FACTORS/CAUSES

Ingestion of contaminated foods
Via skin through contaminated wounds (gunshot wounds or vehicular accident wounds)

SIGNS AND SYMPTOMS

The involved extremity produces foul smelling discharges due to pyogenic formation and is characterized by a thin, brownish body fluid which on slight touch results to emission of bubbles of gas.
The tissues of the wound become greatly swollen, discolored or necrotic (blackish discoloration) and infiltrated with gas.
There is fever, toxemia, shock and later death.

PREVENTION

Serve meals hot, as soon as they are cooked.
Cool foods rapidly, refrigerate until serving time, reheat if necessary.
Early and adequate cleansing of contaminated wounds.
Prompt surgical treatment of wounds.
Administration of antimicrobial drugs directed against clostridia
Gas gangrene antitoxin for suspected wounds.
Passive immunity with gas gangrene antitoxin for deep punctured wounds suspected of being contaminated with Clostridium Perfringens.

TREATMENT

Prompt and extensive surgical debridement of the involved area and excision of all devitalized tissues in which the organism are prone to grow.
Administration of penicillin at the same time.
Hyperbaric oxygen may be of help in the medical management of the clostridia tissue infections.

Photo credit: http://www.graphicshunt.com/health/images/clostridium_perfringens-943.htm