chickenpox, dengue fever, anthrax and personal protective equipment

8/3/2019 Chickenpox, Dengue Fever, Anthrax and Personal Protective Equipment

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Varicella

CHICKEN POX


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Chickenpox is an acute and highly contagious disease of viral etiology that ischaracterized by vesicular eruptions on the skin and mucous membrane with mild

constitutional symptoms.

In unimmunized populations, most people contract chickenpox by age 15, themajority between ages 5 and 9, but all ages can contract it. Chickenpox is usuallymore severe in adults and very young infants than children. Winter and spring are

the most common times of the year for chickenpox to occur.

Chickenpox is very highly contagious. It is easily passed between members offamilies and school classmates through airborne particles, droplets in exhaled air,

and fluid from the blisters or sores. It also can be transmitted indirectly by contactwith articles of clothing and other items exposed to fresh drainage from opensores. Patients are contagious up to five days (more commonly, one to two days)before and five days after the date that their rash appears. When all of the sores

have crusted over, the person is usually no longer contagious.

CHICKENPOX


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CHICKENPOX


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Herpesvirus varicellaea DNA-containing virus

Humans are the only source of infection.

Closely related or identical to herpes zoster virus.

Incubation period is 10 to 21 days or may be prolonged after passiveimmunization against chickenpox.

Period of CommunicabiltyA day before the eruption of the first lesion up to about five days after the

appearance of the last crop

INFECTIOUS AGENT


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Direct with a patient who sheds the virus from the vesicles

Indirect contact, through linens or formites

Airborne, or spread by aerosolized droplets from the nasopharynx of illindividuals

High viral titers in the vesicles of chickenpox; thus, viral transmission mayalso occur through direct contact with these vesicles, although the risk is

lower.

Following primary infection there is usually lifelong protective immunityfrom further episodes of chickenpox

MODE OF TRANSMISSION


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initial inhalation of contaminated respiratory droplets

viral proliferation in regional lymph nodes of the upper respiratory tract

a second round of viral replication occurs in the bodys internal organs, the

liver and the spleen

this secondary viremia is characterized by diffused viral invasion ofcapillary endothelial cells and the epidermis

VZV infection of cells of the Malphigian layer produces both intercellularand intracellular edema

Resulting in the characteristic vesicle

PATHOPHYSIOLOGY


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1. Pre-eruptive manifestations are mild fever and malaise.

2. Eruptive stage

Rash starts on the trunk spreading to the other parts of the body

Initial lesions are distinctively red papules whose contents become milkyand pus-like within four days

In adults and bigger children, the lesions are more widespread and moresevere

There is rapid progression so that transition is completed in six to eight

hours Vesicular lesions are very pruritic.

All stages are present simultaneously before all are covered with scabs,leading to the appearance known as celestial map

CLINICAL MANIFESTATIONS


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The stages are characterized as follows:

Macule = not elevated above the skin surface

Papule = elevated above the skin surface with a diameter of about 3 mm.

Vesicle = pop-like eruption filled with fluid

Pustule = a vesicle that is infected or filled with pus Crust = a scab or an eschar.


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Macule Papule

LESIONS


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Ve s ic le Pustule

LESIONS


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Determination of the V-Z virus

Complement fixation test

Electron microscopic examination of vesicular fluid

DIAGNOSTIC TESTS


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Rarely fatal, although generally more severe in adults than in children

Pregnant women and those with suppressed immune systems are at thehighest risk.

Most common late complication is shingles, caused by reactivation ofvaricella zoster virus decades after the initial episodes of chicken pox

Secondary infection of the lesions- furuncles, cellulitis, skin abscess,erysipelas.

Meningoencephalitis

Pneumonia

Sepsis

COMPLICATIONS


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Oral acyclovir 800mg TID for 5 daysOral antihistamine for pruritus

Calamine lotion for itchiness

Salicylates must NOT be given

Antipyretics for fever

TREATMENT MODALITIES


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Respiratory isolation is a must.

Hygienic care

Diversional activities to lessen pruritus in children

Oral and nasal care

Active immunizations

Isolation

NURSING MANAGEMENT AND

PREVENTIVE MEASURES


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Breakbone Fever/ Hemorrhagic Fever/ Dandy Fever/

Infectious Thrombocytopenic Purpura

DENGUE FEVER


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Dengue fever is a disease caused by a family of viruses that are transmitted bymosquitoes. It is an acute illness of sudden onset that usually follows a benign

course with symptoms such as headache, fever, exhaustion, severe muscle and jointpain, swollen glands (lymphadenopathy), and rash. The presence (the "dengue

triad") of fever, rash, and headache (and other pains) is particularly characteristic

of dengue. Other signs of dengue fever include bleeding gums, severe pain behindthe eyes, and red palms and soles.

Dengue (pronounced DENG-gay) strikes people with low levels of immunity.

Because it is caused by one of four serotypes of virus, it is possible to get dengue

fever multiple times. However, an attack of dengue produces immunity for alifetime to that particular serotype to which the patient was exposed.

Dengue Fever is an acute febrile disease caused by infection with one of the

serotypes of dengue virus, which is transmitted by mosquito genus Aedes.

DENGUE FEVER


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DENGUE


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The bite of an infected mosquito transmits the disease.

AEDES AEGYPTI


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Incubation Period

Three to fourteen days; commonly seven to ten days

Period of Communicability

Patients are usually infective to the mosquito from a day before the febrile periodto the end of it.

The mosquito becomes infective for day 8 to 12 after the blood meal and remainsinfective throughout its life.

Sources of Infection

Infected personsthe virus is present in the blood of patients during the acutephase of the disease and will become a reservoir of the virus, sucked bymosquitoes, which may then transmit the disease.

Standing waterany stagnant water in the household and its premises are usualbreeding places of these mosquitoes.


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Agemay occur at any age, but is common among children and peaksbetween four to nine years old.

Sex- both sexes can be affected

Seasonmore frequent during the rainy season

Locationmore prevalent in urban communities

INCIDENCE


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The infectious virus is deposited in the skin by the vector and initialreplication occurs at the site of infection and in local lymphatic tissues.

Within a few days, viremia occurs, lasting until the 4 th or 5 th day after theonset of symptoms.

Evidence indicates that macrophages are the principal site of replication.

At the site of petechial rash, non-specific changes are noted, which includeendothelial swelling, perivascular edema, and extravasation of blood.

There is marked increase in vascular permeability, hypotension,hemoconcentration, thrombocytopenia with increased platelet

agglutinability, and or moderate disseminated intravascular coagulation.

The most serious pathophysiological abnormality is hypovolemic shockresulting from the increased permeability of the vascular endothelium and

loss of plasma from the intravascular space.

PATHOGENESIS AND PATHOLOGY


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Dengue Fever

Prodromal symptoms characterized by:

Malaise and anorexia up to 12 hours

Fever and chills accompanied by severe frontal headache, ocular pain, myalgia with severe backache and arthralgia

Nausea and vomiting

Fever is non-remitting and persists for three to seven days

Rash is more prominent on the extremities and the trunk. It may involve the face in some isolated cases

Petechiae usually appears near the end of the febrile period and most commonly on the lower extremities.

Dengue Hemorrhagic Fever

Fever, hemorrhagic diathesis, hepatomegaly and hypovolemic shock.

CLINICAL MANIFESTATIONS


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Initial Febrile phase lasting from two to three days

Fever (39-40 Celsius) accompanied by headache

Febrile convulsions may appear

Palms and soles are easily flushed

Positive tourniquet test

Anorexia, vomiting, myalgia

Maculopapular or petechial rash may be present and usually starts in the distal prtion of theextremities. The skin appears purple, with blanched areas of varying site (Hermans sign,

considered pathognomonic to the disease)Generalized or abdominal pain

Hemorrhagic manifestations like (+) tourniquet test, purpura, epistaxis, and gum bleeding maybe present.

PHASES OF THE ILLNESS


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A sign of denguepositive tourniquet test

PETECHIAL RASH


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Circulatory Phase

There is a fall of temperature accompanied by profound circulatory changes, usually on the 3rdto 5th days.

Patient becomes restless, with cool, clammy skin.

Cyanosis is present.

Profound thrombocytopenia accompanies the onset of shock.

Bleeding diathesis may become more severe and lead to GIT hemorrhage.

Shock may occur due to loss of plasma from the intravascular spaces; hemoconcentration with

markedly elevated hematocrit is present.Pulse is rapid and weak; pulse pressure becomes narrow and blood pressure may drop to an

unobtainable level.

Untreated shock may result in coma; metabolic acidosis and death may occur within two days.

With effective therapy, recovery may follow in two to three days.

PHASES OF THE ILLNESS


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Grade I

Fever accompanied with non-specific constitutional symptoms and the onlyhemorrhagic manifestation is a (+) tourniquet test.

Grade II

All signs of Grade I plus spontaneous bleeding from the nose, gumsand GIT are present.

Grade III

There is the presence of circulatory failure, as manifested by a weak pulse,narrow pulse pressure, hypotension, cold, clammy skin and restlessness.

Grade IV

There is profound shock and undetectable blood pressure and pulse.

CLASSIFICATION ACCORDING TO

SEVERITY

(HALSTEAD AND NIMMANITYA)


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Dengue Fever

Epistaxis, menorrhagia

GI bleeding

Concomitant GI disorder

DHF

Metabolic acidosis

Hyperkalemia

Tissue anoxia

Hemorrhage into the CNS or adrenal glands

Uterine bleeding may occur

Myocarditis

Severe manifestations

Dengue encephalopathy is manifested by increasing restlessness, apprehension or anxiety, disturbed sensorium, convulsions,spacity and hyporeflexia.

COMPLICATIONS


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Diagnostic Tests

Tourniquet test

Platelet count

HemoconcentrationOccult blood

Hemoglobin determination

Treatment modalities asymptomatic only

Analgesic drugs

Intravenous infusion to prevent dehydration and for replacement of plasmaBlood transfusion for severe bleeding

Oxygen therapy for patients in shock

Sedatives may be needed to allay anxiety and apprehension

DIAGNOSTIC TESTS AND

TREATMENT MODALITIES


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Because dengue fever is caused by a virus, there is no specific medicine orantibiotic to treat it. For typical dengue, the treatment is purely concerned

with relief of the symptoms (symptomatic). Rest and fluid intake for adequate

hydration is important. Aspirin and nonsteroidal anti-inflammatory drugsshould only be taken under a doctor's supervision because of the possibilityof worsening hemorrhagic complications. Acetaminophen (Tylenol) and

codeine may be given for severe headache and for the joint and muscle pain(myalgia).

Typical dengue is fatal in less than 1% of cases. The acute phase of the illnesswith fever and myalgias lasts about one to two weeks. Convalescence isaccompanied by a feeling of weakness (asthenia), and full recovery often takes

several weeks.


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Keep patient in a mosquito-free environment to avoid further transmission.

Keep patient at rest during bleeding episodes

Monitor vital signs.

In cases of bleeding, act quickly.

Observe for signs of shock.

NURSING MANAGEMENT


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Health education

Early detection and treatment

Eliminate vectors by removing their breeding grounds

Case finding

PREVENTION AND CONTROL


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ANTHRAX


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Anthrax is an infection caused byBacillus anthracisthat occurs primarily inherbivores.

Etiologic AgentBacillus anthracis

It is a large, aerobic, spore-forming, Gram (+), rod-shaped microorganismthat is capsulated and non-motile.

Can survive for years in dry soil but can be destroyed by boiling for 10min.Treatment is done by oxidizing agents such as KMnO4 hydrogen peroxide, or

diluted formaldehyde.

Most are susceptible to penicillin.

ANTHRAX


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An anthrax victim

ANTHRAX


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Anthrax occurs worldwide and is most prevalent among domestic herbivores.Human cases are more resistant to anthrax than herbivorous animals.

Human cases are classified as:

Agricultural cases, which result most often contact with animals that areinfected.

Industrial cases, which are associated with exposure to contaminated hides,

goat hair, wool or bones.

ANTHRAX


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Directthrough contact with infected animals or contaminated animalproducts.

Indirectthrough animal bites and ingestion of contaminated meat.

Airbornethrough inhalation of contaminated or polluted air.

MODE OF TRANSMISSION


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Cutaneous anthrax approximately 95% of human cases

The incubation period ranges from nine hours to two weeks.

a small pimple or macule appears two to three days after the entrance of themicroorganism.

A ring of vesicles develops around the papule. Vesicle fluid may exude

Marked edema starts to develop. Unless there is no secondary infection, there is no pus andthe lesion is not painful, although painful lymph adenitis may occur in the inguinal area.

The original papules ulcerated to form the characteristic of eschar on the 5 th to 7 th days.

Edema extends to some distance of the lesion

Clinical symptoms may be severe if the lesions are located on the face, neck or chest.High fever, toxemia, regional painful lymphadenopathy, and extensive edema. Shock and

death may also ensue.

TYPES OF ANTHRAX


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CUTANEOUS ANTHRAX


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Inhalational anthrax (woolsorters disease) 5% of cases

Symptoms resemble those of severe viral respiratory disease.

After 3 days, increasing fever, dyspnea, stridor, hypoxia and hypotension occur, usually leading todeath within 24 hours.

Organisms are deposited into the alveoli or into alveolar ducts, producing hemorrhagic necrosisof nodes associated with hemorrhagic mediastinitis.

Gastrointestinal anthraxresults from ingestion of inadequately cooked meat from animals withanthrax.

Occurs in the intestines where lesions are formed, accompanied by hemorrhagic lymphadenitis.

Fever, nausea and vomiting, abdominal pain, bloody diarrhea and sometimes rapidly developingascitis.

TYPES OF ANTHRAX


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Inhalat ional Gastrointest ina l

ANTHRAX


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Anthrax meningitis is the intense inflammation of the meninges of thebrain and spinal cord.

Elevated CSF pressure with bloody CSF, followed by rapidly loss of

consciousness and death.Fatality rate is almost 100 percent.

Anthrax sepsis develops after the lymphohematogenous spread from theprimary lesion.

High fever, toxemia and shock, with death following in a short time.

COMPLICATIONS


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Parenteral penicillin G2 million units every 6 hours, until edema subsides,with subsequent administration of oral penicillin for a 7 to 10 course.

Patients who are sensitive to penicillin can be treated with erythromycin,tetracycline, or chloramphenicol.

Nursing management

Careful history taking

Thorough physical examination

Skin care, psychological, and emotional supportSupportive measures are geared toward the type of anthrax exposure

Any type of anthrax should be reported to health authorities.

TREATMENT AND MANAGEMENT


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PERSONAL PROTECTIVE

EQUIPMENTS


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Personal protective equipment (PPE) is used by healthcare providers toprotect themselves from injury or infection. There is personal protective

equipment to keep rescuers safe from physical injuries, from chemical hazards,and from infection. Lay rescuers should follow their professional counterpartsby practicing universal precautions and using PPE to provide protection from

infection when assisting victims in an emergency.

PPE


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The best way to prevent the spread of disease is to wash hands with soap and warm waterafter every contact with a medical victim. Unfortunately, soap and water are not always

available. Make sure your medical supplies include a form of waterless hand cleaner.

HAND CLEANERS


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Exam gloves come in three common types: latex, nitrile, and vinyl. Many peopledevelop allergies to the protein found in latex. Nitrile and vinyl are much more

hypoallergenic. Find out more about exam gloves.

GLOVES


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Many lay rescuers do not want to perform the rescue breathing part of CPR because of theclose contact required with the victim. The best way to avoid that squeamish feeling is to be

prepared. CPR masks provide an important barrier between rescuer and victim.

CPR MASKS


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Blood or other potentially infectious material sprayed or splashed in the face ofa rescuer can enter the mouth or nose and spread an infection. Use a face mask

whenever blood or other body fluids may become airborne.

FACE MASKS


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Protect your eyes from injury as well as infection by obtaining the correct type of eyeprotection. Rescuers can choose from combination mask and eye protection that does not

provide protection from injury, or they can choose more robust protection. Pick the correcteye protection for you.

EYE PROTECTION


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Contaminated sharps must be deposited into a puncture-proof container. These

containers protect sanitation workers from injury as well as other rescuers.

SHARPS CONTAINER


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Full-body gowns are not used very often outside of the hospital. There is no goodreason for this, it is just common practice across the country. Put the correct gown in

your first aid kit and avoid the need to dispose of your favorite shirt or blouse.

GOWNS


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Contaminated waste should be placed into a red, bio-hazardous waste container to distinguishit from regular garbage. When working with an ambulance, it is common for the ambulance

crew to allow lay rescuers to dispose of their contaminated items in the ambulance's bio-hazard container.

BIOHAZARDOUS WASTE


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PREVENTION IS BETTER THAN

CURE.

Desiderius Erasmus


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THANK YOU!Caberte, Mae Lyn M., Group 20

chickenpox, dengue fever, anthrax and personal protective equipment

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