Nursing Case Study Dhf Dengue Hemorrhagic Fever

8/2/2019 Nursing Case Study Dhf Dengue Hemorrhagic Fever

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~ ~ I T i l ~ ~ ~ ~ I T i l @ ~ ~ ~ ~ I T i l ~ D @ @ l l i J i l~ ~ ~ ~ I T i l ~ ~ ~ ~ I T i l @ ~ ~ ~ ~ I T i l ~ D @ @ l l i J i

DENGUE HEMORRHAGIC FEVER:A Case p ~ ~ I T ~ m ~ ~ ~ I T i l @ ~ ~ ~ ~ I T i l ~ D @ @ l l i J i l

~ ~ ~ ~ I T i l ~ ~ ~ I T i l @ ~ ~ ~ ~ I T i l ~ D @ @ l l i J i l~ ~ ~ ~ I T i l ~ ~ ~ ~ I T i l @ ~ ~ ~ ~ I T i l ~ D @ @ l l i J

~ ~ I T i l ~ ~ ~ I T i l @ ~ ~ ~ ~ I T i l ~ D @ @ l l i J i lGroup p ~ m r ~ ~ ~ ~ ~ I T i l @ ~ ~ ~ ~ I T i l ~ D @ @ l l i J i l

Submitte d to


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Dengue hemorrhagic fever (DHF) is an increasing public health problem and it has been known for morethan a century i.nthe tropical areas of the South-Ea~~nhfFffii(J~~m1~rw1~ITiJ~D@ITili)Philippines, DHF was first recognized in 1953 whilJ.ii{ltWal~~~~~S' illW$~.~~m~~ry concerningthe causative agent was solved when dengue virus types 2, 3, and 4 were isolated in the Philippines in1956 and dengue virus type 1 in Thailand in 1958.

dengue virus (family Arbovirus, genus Flavivirus) and characterized clinically by a hemorrhagicdiathesis and a tendency to develop a shock syndro~ ~5ff~hOck syn&ome- DS~ tha~ay be f~al.Thrombocytopenia with concurrent hemoconcentraWU~~i:llittOO_@~1JlliJW@[JiJUD@@ITili)

The clinical features of dengue fever frequently depend on the age of the patient. Infants and young~ D~~dren m.a.ycr-ave an U1~i~~r.:.rr~ed f~rile disease with a maculo-papular rash. Older children and

~ U U ~ LH:ru@]?~~.~~[ili~~~assical incapacitating disease with abrupt onsetand high fever, severe headache, pain behind the eyes, muscle and joint pains, and rash. Skinhemorrhages (with a positive tourniquet test and/or petechiae) are common. Leukopenia is usually

Many epidemics of dengue fever are accompanied by bleeding complications such as epistaxis (nose-bleeding), gingival bleeding, gastrointestinal bleeding, hematuria (blood in urine) and hyperrnenorrhea.

manifestations: fi:1ghfever, hemorrhagic phenomena, hepatomegaly, and, often, circulatory failure.Moderate to marked thrombocytopenia with concomitant hemoconcentration is a distinctive clinicallaboratory finding. The major pathophysiological c~ R14~~~ fl~rn~ [email protected])dengue hemorrhagic fever (DHF), and differentiatewllUWU~~~~@~ ~~\:7manifested by a rising hematocrit value and hemoconcentration.


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( . ~ ~ n ~ ~ ~ ~ ~ : : d s y m p t o m sn d e n g u e~ ~ I ~ ~ ~ ~ ~ ~ i~ t r @ @ T ~ ~ D @ @ l l i i l l.:. To examine associations between DHF incidence pattern with demographic,

environmental factors and DHF control activities.~~~ll i l:.~ToclDeab~eto ~ 0 r g F t :tiol~y and ;owthe mode of transmission takes place.~. ~~lID~~Jl~~~ID]hl~~~ijSiOlogy of the hematologic system..:. To be able to know what course of action is done by the virus causing DHF .:. To disseminate needed information on ~ O ~ ~ ~ f f i } ~ Q ~ @ o u Q D @ @ l l i i l lImportance and dangers. W U t : : J U U ~ \ : : : /.:. To be able to formulate pertinent nursing care plans that will be useful in the

D man~ement ofDHFIt:e: s .~ ~ ~ ~ I T il l I D ~ ~ [ J Y ~ ~ ~ I ! P i & _ i d e r a t i o n o f t h e d r u g st a k e n b y p a t i e n t sw i t hDHF.

:. To be able to develop helpful and applicable health teachings that will guide clients bothi n t r e a t m e n t n d p r e v e n t i o n f D H F . ~ ~ ~ ~ I T i l [ l j J ~ ~ ~ I T i l@ ~ ~ [ l j J ~ @ I T i l ~ D @ @ l l i i l l


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~ ~ [ i l l [ lD~ ~ [ i \ ] ~ U [ lD ~ [ i \ ] U D @ @ ll i l i lTheoretical Framework

Jean Watson's Human Caring Theon)Dengue haemorrhagic fever (DHF) is a potentially deadly, if not debilitating, disease.

vaccineforDengue ' " TUS , supportive therapywill be a good course to carry out among patients inflicted with such ailment. Thus, the groupselected lean Watson's Hum an C arin g n"oly b c ~ IT ~ m ~ M t l~ ~ [ i \ ]U D @ @ ll i l i lnursing care management towards the recovery of patients with DHF. Jean Watson strongly

believed that providing protective, supportive or corrective mental, physic at socio-cultural, and~~~~rntf~.@~~n@@~sable factor for successfulrecuperation.


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FEVER & THE HYPOTHALAMUS

Fever,alsoknown aspyrexia, is the rise intheb O d ~ ~ ~ O O @ ~ ~ @ @ l l i l i lmany disorders, SUd1 as infection by a virus or a bacterium, and it is not itself a disease. The first signs offever may be chilly sensations, with associated periods of flushed or warm feelings. The temperature may

may be accompaniedby shakingchills.A

Although people have survived temperatures over 430 C (110 na fever higher than 410 C (106 F)typically results inconvulsions, particularly in b a b i ~ r n ~r Q U ~ ~ ~ ~ O U @ ~ ~ Q j J ~ O U ~ DFever can be classified as:

Low-grade: 38-39C

Hyperpyrexia/hyperthermia: 42C or more 0 0Thenormal healthy body constantly produces heat ~ ~ ~ b l ! l D ~ ~ ~ ~ D @ @ l l i l i lbody loses heat through the skin and through breathing. The temperature of the body is a measure of thebalance between heat produced and heat lost. Under normal circumstances the heat produced is balancedby the heat lost, keeping the body temperature at the best level for the cells to carry out their chemical

~ ~~OO~ft~~~n~BTI~B@~be upset by bacterial or viral infections, such as1 to~itis orY~l1Jib1~ ktWe~c~s, protein~~li~ ~yrogens are released when the white blood cells ofthe body's defense system fight the microorganisms responsible for the illness. In some cases thepyrogens are released by the microorganisms them~~~~rW.IWs aD: on ~e~.on~aMt0 .. s, a s~allarea of the brain that functions as a thermometer, ctfM8IQ ~ ~ g ~ ~ ~ W ~ o @ lli l i ltemperature is rising, the tiny vessels supplying the skin with blood can narrow, sharply reducingsweating, which is a way for body heat to escape. The body will thus produce more heat than it can lose,


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brain's thalamus and above the pituitary gland. The hypothalamus is divided into several distinct nuclei,that is, aggregates of nerve cell bodies. These nerves connect the brain with the hypothalamus and the1 n I~ ~ ~ffn~rrnrm~~~~~~~e rlJ~tem. The hypothalamus also receives nerve

~ ~~~M!fMW~~~~(lt?JJ~~th(1ili~leS), the viscera (internal organs), and the limbicsystem (concerned with motivation and drive).

autonomic nervous system. Fear or excitement causes signals to travel to the hypothalamus, whichtriggers a rapid heartbeat, faster breathing, widening of the pupils, and increased blood flow. The~ ~~M ~ ~ ~ :@ i b O d Y 'S water content ro regulate appetite for rood0The hypothalamus also plays an important role in regulating feeding behavior. Experiments performedon rats demonstrate that if the middle of the hypOth~~~M damaged., t~ rat ove.re~F1~~~meh . _obese; damage illthe lower part causes the rat to re~ ~M~f?@q~~~[flJ ~ D @ W Uhypothalamus is less important than in rodents because conscious decisions playa greater part inhumanprocesses such as eating and drinking. For example, it has been shown that custom and habit have agreater influence over the amount eaten than actual hunger.


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~ 0 n Moreover.jne hffiors~~~~n be r~arded as the thermostat controlling the temperature of the body.U ~ U [i100~~~~R@~tm@.@hlW,lood vessels. The hypothalamus triggers behaviors

such as putting on or removing clothes, turning on the heat, or moving into the shade.

HUMAN IMMUNE SYSTEMn ~ M ll~(c$~r,H~f1JAfi~~.~tV,)ro~~~nfeCtiOUS microorganisms ~y means of a complexU lliJIJlWs~1l1~~~hlll~~l.J,~the surface pattern of the Invader. The two parts ofthe system are termed cellular immunity, in which lymphocytes are the effective agent, and humoralimmunity, based on the action of antibody molecules. The health of the body is dependent on theimmune system's ability to recognize and then , ~ p e ! P ~ ~ f f i 1 l @ ~ ~ Q l ] ~ l l i l ~ D @ @ l l i l i lMost animals have systems that resist disease. The disease resistance provided by these systems is calledimmunity. There are two types of immunity: innate and adaptive. Innate, or nonspecific, immunity is thern I~ ~~rff1~mm~rcr~4a~nh~ers. Innate immunity is furnished by barriersl? ~ U ~ ~sl~WJJJJ~~~~WJ)ll~~~aPid inflammation of tissues that takes placeshortly after injury or infection. These innate immune mechanisms hinder the entrance and spread ofdisease but can rarely prevent disease completely.

rr a n invader g e f f i a s tthis f i r s t i n e o fdefense, t h e c e W Q u ~ I , l i l l ~ ~ [ ~ ~ ~ 1 l i l l ~ ~ j ~ D @ @ l l i l i ldevelop specifically tailored defenses against the invader. The immune system can call upon these

defenses whenever this particular invader attacks again in the future. These specifically adapted defenses

Adapti ve immunity has four distinguishing properties: First, it responds onl y after the invader is present.

a n m :a . " . v ~ ~ ~ U _ D @ @ l l i l i lecond, it is specific, tailoring each response to actmemory, responding better after the first exposurelater. Fourth, it does not usually attack normal body components, only those substances it recognizes asnon-self.


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~ 0 n Adaptive iIDffiune res~~s~~e oactu~ reactions of the immune system to structures on the surface ofU ~ U [MMbf~~~~~~@_types of adaptive immune responses: humoral and

cell mediated. During humoral immune responses, proteins called antibodies, which can stick to and destroyantigens, appear in the blood and other body fluids. Humoral immune responses resist invaders that actoutside Of.cells, such as bacteria and toxins (Poi~onmlIDTIfi~~flW~OOm01J~D@[]ili)Humoral immune responses can also prevent vlrusU1rom en~e~~~elit.U UU~~ L JDuring cell-mediated immune responses, cells that can destroy other cells become active. Their destructive

~ 0n adivitNs liBrited to ce~Nh~rn\ithel1nfected ~ or producing, a specific antigen. Cell-mediatedu 1]~lm~~ij~lli)~i1@@LH:H!pin the body cells, such as viruses. Cell-mediatedresponses may also destroy cells making mutated (changed) forms of normal molecules, as in somecancers.

interactions between the components of the immune system and the antigens on the invading pathogens,or disease-causing agents.~ ~ ~ m ~ g~ ~ ~. Some white blood cells, known os macrophagee,playa function in innate immunity by surrounding, ingesting, and destroying invading bacteria andother foreign organisms ina process called phagocytosis (literally, "cell eating"), which is part of theinflammatory "action. Macrophage> aleo play an ;m~~F'i!11l1'1~fI~~~D@[]ili)to invading antigens and deliver them to be destroye~yU~hle~~~lJe~lbY y~&t 'p~~~~U U l)[ .system.


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lymphocytes regula

~~o~~ytes are specialized white blood cells that identify and destroy~~~tlm~:~:7~~HEYtes directly destroy invading organisms, whereas other T

e immune system by directing immune responses.

Lymphocytes are specialized white blood cellswh~~~tm~~~~~~o@lliillantigens. All lymphocytes begin as "stem cells" in t U; b~ ~e m a rr ow , the soft ~s~~~hat fillsmost bonecavities, but they mature in two different places. Some lymphocytes mature in the bone marrow and arecalledBlymphocytes. B l ymphoc yt es , or B c ells ,make antibodies, which circulate through the blood and~m ~ ~ f f i 1 ~ ~ ~ ~ g @ @ m e " r o y them inhumoral immune m'pon",.When particular lymphocytes recognize a foreignmolecular pattern (termed an antigen), they releaseantibodies in great numbers; other lymphocytes store the noerf~ryof the..P8ttcm fo.ru. tu . re release ofantibodies should the molecule reappear. AntibOdie~~tftrtJOOWS@~~o@lliillmark them for destruction by other substances inth~oUd~ defense arsen~~~~~e primarilycomplement, a complexof enzymes that make holes in foreign cells,and phagocytes, cells that engulf and

Lymphocytes, which resemble blood plasma in composition, aremanufactured in the bonemarrow andmultiply in the thymus and spleen. They circulatein the ~~tream, penelfftting the 'If;~sn0;tr: bloo{\,capillaries to reach the cellsof the tissues. From there~_~W~OO~~[]1J\jD@lliillcapillaries that is comparable to and almost as extensive as that ofthe blood's circulatory system. Thecapillaries join to form larger and larger vessels that eventually link up with the bloodstream through thejugular and subclavian veins; valves in the lymphatic vessels ensure flow in one direction.Nodes at

~ ~ ~ in i I1f i i f '~ft~i$nr I l~@rr; ,~ afF3m1fflms for the collectionand manufacture ofl l1~hb~kWM~)~~~~JitttWtP~~YirJMfectiOUS disease. In anatomy, the network oflymphatic vessels and the lymph nodes are together called the lymphatic system; its function as thevehicle ofthe immune systemwas not recognized ~ m J ~ I T I 6 0 S ~ ~ ~ [ f i ] 0 .. ' ~@ ~D@@lliillOther lymphocytes, called T ly"'phocy l'G , 0T cells, mtme in ~ ~ymVS' a s m m , ~ i l l ,,gan@catedbehind the breastbone. SomeT lymphocytes, called cytotoxic (cell-poisoning)or k il le r T l ymphoc yt es ,generate cell-mediated immune responses, directly destroying cells that have specificantigens on their


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~ 0 n surface thatjare recog~~dn?n~ ~T I~ cells. Helper T lymphocytes, a sec~nd kind of Tlymphocyte,U ~ UUQOO~~Q.~~~j\~tH~1[]~th and quality of all immune responses.

Most contact between antigens and lymphocytes occurs in the lymphoid organs-the lymph nodes, spleen,and tonsils, as well as specialized areas of the intest~~~fl~rf140~~~~mrfr1!f~ ~lymphocytes constantly travel through the blood to[ftUYill~~a~!JUli~bklMJ~~lliJ l j o @ U i l i )again. This recirculation ensures that the body is continuously monitored for invading substances.

~ o n One.ofthell"uacte~A of jfPti:..~un. ity.is that it is specific: Each response is tailored to a specificU U ~ U _~~I]jt!U@~D@~res, makes an antigen receptor-that is, a specific

structur~~i~sUs~ace that can bind with a matching structure on the antigen like a lock and key.Although lymphocytes can make billions of different kinds of antigen receptors, each individual

When an antigen enters a body cell, certain transport molecules within the cell attach themselves to thern I~ ~~fflt~~~M11~~~e ~~~ they "present" the antigen to T lymphocytes.l? l 1 i j U ~ n i j J U l J ~ ~ l b ~ ~ ~ ~ l L l ~ \ Q f ~ W s called the major histocompatibility complex(MHC) and are therefore known as MHC molecules. Some MHC molecules, called class IMHC molecules,present antigens to killer T cells; other MHC molecules, called class II MHC molecules, present antigens tohelper T cells. ~~~ ~ l l i l [ i l l ~ ~ ~ l l i l ~ ~ ~ l l i l~ @ l l i l~ D @ @ U i lHumoral Immune Response

macrophages take up some of the antigen and attach it to class II MHC molecules, which then present theantigen to T helper cells. The T helper cells bind the presented antigen, which stimulates the T helper cellsto divide and secrete stimulatory molecules called i ~ ~ ~ ~ ~ M ~ _ o @ U i l i )lymphocytes that have also bound the antigen. The ~~~ted B cells then ~i~~~d secrete antibodies.Finally, the secreted antibodies bind the antigen and help destroy it.


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~ 0 n AntibOd. ieUl.~~. -sh0!ap~P~~in: call~.' .inununoglobulins (Ig) and are made only by B cells.. TheU ~ UWW~~g[l~~~@OO~U@~)f the Y. The area at the base of the Y determineshow the antibody will destroy the antigen. This area is used to categorize antibodies into five mainclasses: IgM, IgG, IgA, IgD, and IgE. During the humoral immune response, IgM is the first class ofantibody made. ~fter several days, other classes aPfM~~~fTn~~~~~D@@[fUlJdepends on the kmd of interleukins It receives froJii{eutJ~e~~e~~s. UUU~~ L JAntibodies can sometimes stop an antigen's disease-causing activities simply by neutralization-that is, by

~ 0n ~nndlf~ thElJl~~Rf11Hh~~9-i!.N~m in~~ with the cell's normal activities. For example, theU U ~ Uu~~Q~ ~ ~ ~ ~ ~ t h interferes with their control of muscles.Antibodies against tetanus toxin stick to the toxin and cover the part of it that binds to nerve cells,thereby preventing serious disease. All classes of antibodies can neutralize antigens.

Antibodies also help destroy antigens by preparing ~1Qlllili?~~~llil~~lJil~D@@[fUlJcalled opsonization. In opsonizaiion, antibodies coat the surface of antigens. Since macrophages havereceptors that stick to the base of the antibody's Y structure, antigens coated with antibodies are more

Finally, IgM and IgG antibodies can trigger the complement system, a group of proteins that cause cells todisintegrate by cutting holes in the cell membrane. C I 0 r f f 1 ~ T I ~ ~ m m 1 _ @@[fUlJhard to destroy in other ways. For example, some of t e oactenH~~~u~ pJ-le~~~ ~ave ~imy 0 0coating, making it hard for macrophages to ingest and eliminate them. However, if IgM and IgGantibodies bind to the pneumonia bacteria and activate the complement system, it is able to cut holes in

~~~~~1?~~t~c~cr~~ITO~D@@[fUlJAlthough the Ib~ d TgGclasses of antibodies work best in the circulatory system, IgA can exit thebloodstream and appear in other body fluids. IgA is thus important in preventing infection at mucosalsurf~ces, s~ch as th,e intestine and ~e lung. Since thr0~rTFrf.sites whenilnos~~~us aIgA IS particularly Important 111 resistance to many ~ . f J l . u ~ r n J ~ ~ Q W ~ . . .help nursing newborns resist disease.


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~ ~ ~ l i I ~ ~ Q i j 1 i l i t 5 t : d = : : :: : ' : : t : : V : : : :: : : : : : : : ;by macrophages and presented to helper T cells. The helper T cells bind the presented antigen andthereby become activated to divide and secrete interleukins. The interleukins in tum activate any killer Tcells that have already bound antigen attached to c l~~f f fW?~~a. rnTnQ~fu @[]ili)killer T cells can then kill any cells displaying antigJKa~t~~l~~ U~a~s ~(:l~ecu~~~c'ti?e~~ 0eliminating any cells infected with the antigen.

~ D n 0 f i ~ ~U U U . ' 0 ' o . 'g . ays pass before the adaptive immune response~ ~ . f ] J l ~ ,g,WemiIWand falls, During following exposures to the sameantigen, the immune system responds much more quickly and reaches higher levels. Because the first, orprimaru, immune response is slow, it cannot prevent~11;~n'llthough it.li)1y hel.p it.l~~~e;n In Acontrast, subsequent, or secondary, immune responsWOOUH_~~~~:@~\:~1:j@@[]ili)detected, attacked, and destroyed before symptoms appear. This complete resistance to disease is calledimmunity and may be achieved through either active or passive immunization,

Blood is the vital fluid found in humans and other ain'rru t~~ provides imB0rtant ~.A~~:Wo allbody organs and tissues and carries away waste mat r { ) l ~ ~ f f i J @ B ~ f i @ ~~fi1)~D@[]ili)blood is pumped hom the heart through a network 0 lood vessels 0 0 1 1 ective~wn as the circulatorysystem.

ut 5 ~~Al to 2 gal) of blood, which is roughly 7 to 8 percent of total bodya ~@@~olumes of blood, roughly proportionate to theirrunning a marathon, blood volume decreases. Blood volume increases in circumstances such as


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~~~:[~~~m,~~P~~@~~ri~t~!funnatiO~;t is also responsible for the activities ofthe immune system, helping fend off infection and fight disease. In addition, blood carries the means forstopping i.tse.lfrom leaking out of t~e body after ~~~rtrR~~~s~~~~~11r ( r )@ ~and proteins, known as the coagulation system, thatriliUtU l J l i l J . . U t l J J , ~ ~ ~ ~ U ~ J b D \ : : : 7 U U Uinjury.

r l - t 0 n BlOO:dis vite} to m.a;nt'ie'~ ~ ; . ' : I : : ; : l t yte.mp.erature; in humans, body temperature normallyI U ~ UWOO~~~~~1J@@Hiftrduction and heat loss in various parts of the bodyare balanced ~~t~~at transfer via the bloodstream. This is accomplished by varying the diameter ofblood vessels in the skin. When a person becomes overheated, the vessels dilate and an increased volumeof blood flows through the 00n. Heat dissipates thr~I'!,'j~~~y;;1r';;./" f r : j@ ~temperature. The increased flow of blood in the sknt_r{JJJJUJJW~ 1 P ~ ~ ~ ~ ~ W ~D\::7 . U U Uperson is cold, the skin may become pale as the vessels narrow, diverting blood from the skin and

reducing heat loss.

About 55 percent of the blood is composed of a liquid known as plasma. The rest of the blood is made ofthree major types of cells: red blood cells (also knownrmfru_im~rmffll~OO~_D@@Uili)platelets (thrombocytes). l ? ' ~Plasma consists predominantly of water and salts. The kidneys carefully maintain the salt concentrationin plasma because small changes in its concentration will cause cells in the body to function improperly.O O M f ~ ~ ~ ~ ~ ~ ~ @ f f i I D ' or even death. The pH of plasma, the common' measuremenY ~~~asma/s acidity, is also carefully controlled by the kidneys within the neutral rangeof 6.S to 7.7. Plasma also contains other small molecules, including vitamins, minerals, nutrients, and

waste products. The concentrations of all of these m~e~ITrlli)llir~r~~~tm@[ill~D@@Uili)

Plasma isusually yellow incolo, due to proteins dlmlved in it.However, afte~;'"on cats a fattymeal, that person's plasma temporarily develops a milky color as the blood carries the ingested fats fromthe intestines to other organs of the body.


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~ 0 n Plasma carries a lar~IT~~m~ imJ1ani:\roteins, including albumin, gamma globulin, and clottingU ~ U OO:~~~~@i l l l l i f l~_ regulate the water content of tissues and blood.Gamma globulin is composed of tens of thousands of unique antibody molecules. Antibodies neutralizeor help destroy infectious organisms. Each antibody is designed to target one specific invading organism.For example, chicken pox antibody will target ChickJWl~~~R~~M~~~ @UDUunharmed. Clotting factors, such as fibrinogen, are b V v ~ ~ ~ J 1 ~o~~fiM~JJ ~~~ se~~~1.~er ~ninjury. Plasma that has had the clotting factors removed is called serum. Both serum and plasma are easyto store and ha ve many medical uses.

oxygen from the lungs to every cell in the body. Red blood cells are composed predominantly of a proteinand iron compound, called hemoglobin, that captures oxygen molecules as the blood moves through thelungs, giving blood its red color. As blood passes thfffi~mw~~@:~~eTIQD@UDUoxygen to cells throughout the body. Red blood cell~e so packe~vitl~~~OU~~ tl~at they lack.manycomponents, including a nucleus, found in other cells.

IiiIn :, n ~ n~APm'11~~IO~~~Xihlc, like a soap bubble. and" able to bend inl _ f l U U u lillcUl~JM~W~~~~WlJJ~WJU~bbause the red blood cells must be able to pass

through the tiniest blood vessels, the capillaries, to deliver oxygen wherever it is needed. The capillariesare so narrow that the red blood cells, normally shaped like a disk with a concave top and bottom, mustbend and twist to maneuver single file through them.~~~ ~ [nJ[m~~ [nJ~~~Q!]~@[nJ~D@UDU

White blood cells only make up about 1 percent of blood, but their small number belies their immenseimportance. They playa vital role in the body's immune system -the primary defense mechanism

~ 0 n against invEiding bactett:~ ~i::.rr6 ~r! ; and parasites. They often accomplish this goal through directU ~ U OO@1?@.~~~\{~~"g organism as foreign, attaching to it, and thendestroying it. This process is referred to as phagocytosis.

White blood cells also produce antibodies, which a~ ~~i1'rl~ @UDUattach to foreign organisms. After attachment, the a~~Y l l iJ Y ~ . l l iJ U ~ ~ ~ ~ ~ ~ ~ U ~help from other immune system cells to destroy the foreign substance. There are several varieties of whiteblood cells, including neutrophile, monocytes, and lymphocytes, all of which interact with one anotherand with plasma proteins and other cell types to form the complex and highly effective immune system.


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~ ~~ a . ~ Q lJ .T"'V d",'''' lnacttvated, about 250,000 P" cublc mm ofblood, unt il they come into contact with a damaged blood vessel. At this point, the platelets form a clump, adhering to each otherand to the blood vessel wall. They secrete chemicals that alter a blood-borne protein, fibr inogen, so that it forms a mesh of f ibers atthe damage site. A clot forms when platelets and red and white blood cells become trapped in the fibers. Blood clot tlnq beginswithin seconds of injury. Th, same process can produce '"w"wm~ r n O O ~ Q 1 l ~ ~ ~ ~ @ ~ ~ Q J ] ~ @ I T U ~ D @ @ W UThe smallest cells in the blood Me the p late Iets Whi~are designed for a single purpose - to begin theprocess of coagulation, or forming a clot, whenever a blood vessel is broken. As soon as an artery or vein~~fi th~lateleffi .'vessels to reduce b eeding, attracting more platelets to the area to enlarge the platelet plug, and initiating

of the ~jury begin to clump together and stick to the edges of the cut.~B@_a variety of functions: constricting the bloodthe work of plasma-based clotting factors, such as fibrinogen. Through a complex mechanism involvingmany steps and many clotting factors, the plasma prcm~~~_~~~UU0 @ W Uthreads of fibrin. Together, the platelets and the fibru&e~~~W Y-MM~.Yl.ll~~e~~ ~~~s a sfa~Jlclot. This self-sealing aspect of the blood is crucial to survival.

Production &Elimination of Blood Cells~~~Til[lli~_D~J.ij] central cavity inside almost all of the hones in thebody. In infants, the marrow in most of the bones is actively involved in blood cell formation. By lateradult life active blood cell formation gradually ceases 1'1-:~ones of the If"'" and lef\ ,",~ncentmtesinthe skull, spine, ribs, and pelvis. ~ l f U ~ U I T U Q J ] ~ ~ ~T U @ ~ u Q J ] W I T U ~ D @ @ W URed blood cells, white blood cells, and platelets grow from a single precursor cell, known as ahematopoietic stem cell. Remarkably, experiments have suggested that as few as 10 stem cells can, in


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Red blood cells have the longest average life span of any of the cellular elements of blood. A red bloodcell lives 100 to 120 days after being released from t~mffi~ffnM~~~96i~rfn?tf6{~ f r j@~red blood cells gradually age. Spent cells are remov~tJ~~L!~~~~WhD\2:::7 U U UThe spleen and the liver also remove any red blood cells that become damaged, regardless of their age.The body efficiently recycles many components of the damaged cells, including parts of the hemoglobin

~~~~otroUIT~v~UMw@UDtr~t@lli1OThe majority oh~te blood cells have a relatively short life 'pm,. They may survi ve only 18 to 36 hoursafter being released from the marrow. However, some of the white blood cells are responsible formaintaining what is called immunologic memory. m~~r f f1~FcS~~t f~ t J \ r , ; l~ ( ( 0 @ ~infectious organisms the body has previously been ~ W J ~ U J J ~ b' tJJ l fn{~UlJ,~~~~~lJ l!JD~ 0 U U Umemory cells initiate an extremely rapid response designed to kill the foreign invader. Memory cells may

live for years or even decades before dying.

~~~_ ~~iZatiO" also called a vaccination", oninoculation, is a method of using a vaccine to make the human body immune to certain diseases. Avaccine consists of an infectious agent that has been weakened or killed in the laboratory so that it cannotproduce disease when injected into a person, but can ~~~~f t t ID~~~~ @@lli1Oand antibodies specific for the infectious agent. If the Wel.Jt~ousY~eWsliJtrf~ eve~WJ.J~~a~~a~e~Dperson in the future, these memory cells will direct the cells of the immune system to target the invaderbefore it has the opportunity to cause harm.

rnJM_~~~~mrug@ITOOoOd. They either participate in clot formationl during that tim~, when they have reached the end of their lifetime, are eliminated by the spleen and, toa lesser extent, by the liver.


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~ 0 ~ p a t h m h T I 1 i O l ~ @ ~ 0 J ~l n r r ; J n n ~ r;;l 0 n n 0 io\rJ@@8iteofBdengUe-V;mS(DEl'.1-IIDEN_-2IDEN-3IDEN-4)-U U U W C V U U W \ . . 5 'U U D mfected femaleAedes


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Nursing Cues / Planningrationalessessment

-Client' 5 temperatureIIAng sakit-sakit ng uloko, parang umakyatIahat ng init sa ulo ko."

decreased to 37.6DC

-patient's subsequent her headache recededObject ive: headache will subside

-Patient was able toremote body surface breathe normally

when touched pattern will improve or cooling by means ofTachycardia normalize

@ l li il l

undressing; cool~~J~~J~ ~ Q D ~ @ I T i l ~ D @ l li il lNursing Diagnosis 1:

packs, particularly ingroin & axillae sincethese are areas afhigh

"Subiectiue: -Patient's risk for fluid -Weigh client & -Patient did notdeficit will be prevented compare with recent undergo fluid volume

@ l li il l


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weight history to deficitd ete rm in e a ny lo ss es

A risk diagnosis is not -Encourage oralm " , . ~ r n J ~ ~ [ 1 j ]~ @ [ f l ]~ D @ [J U iJevidenced by signs &symptoms, as the problem hasnot occurred &nursinginterventions are directed atprevention.

balance being aware ofinsensible losses toe ns ur e a c cu ra te p ic tu re o f

N urs in g D ia gn os is 2 :Risk for deficient fluidvolume related to -Assess skin turgor/oralexcessive losses throughvomiting

~ ~ ~ [ f l ] [ 1 j ]~ ~ ~ [ f l ]@ ~ [1 j ]~ @ [ f l ]~ D @

Subjective:Patient stated her loss of -A nutritional plan that -Assist in developing

individualized regimento correct/control

-Patient was able toappetite and interest in meets patient's needs t m ~ ~ - consume her mealsObjective: -Patient will be able toBody weight 25% below eat at least 3 times a daythe ideal, considering

.. u nd er ly in g c au sa ti vecompletely, 3 times aday.

frame;-Patient will gain atleast 4 pounds

indicated t o imp lemen ti nt er di sc ip li n ar y t eam -Patient's general

patient's height &

Poor muscle tone; managemen t appearance improved


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appealing to stimulateD ~ I T U [ i l l ~ ~ I T U ~ ~ [ i l l W I T U ~ D @ I T U Umucous membranes

vsical.@ @

Nursing Diagnosis 3:

enhanced

Imbalanced Nutrition:Less than body

-Encourage client tochoose foods that are

-Promote pleasant,relaxing environment,including socializationwhen possible to enhance

Drug Study

Date Medicationffreahnent Actions Indication Nursing Consideration

650mg PO q4 hrProstaglandins thatmay serve asmediators of pain& fever, prima~inthe CNS. Ith Wno significant anti-inflammatoryproperties or GItoxicity.~ ~ ~ ~ m [0 l l i l@ [0 ~ [ l l ] ~ l l i lAntipyresis

.1l~"P'U"'~~antipyretics,nonoploidanalgesics

Assess amount, frequency,and type of drugs taken inpatients self-medicating, esp.with OTC drugs. Prolongeduse of acetaminophen alone orcombined with salicylates orNSAlDs increases the risk of~ l l i l [ l l ] ~ [ 0~~frD @ I T U Uacetaminophen and salicvlatesshould not exceed therecommended dose of either

Mild pain,Fever

=Assess overall health status &alcohol usage beforeadministering acetaminophen.Malnourished patients or

~.,ron~ t r b C I . U S ~ ~ ~~~Xlclt;m~rOll.lc useof usual doses of this drug.

@ I T U U


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Albumin (human) Provides colloidal~~~~m~ ~~~ILextr avascular

administration ofappropriatec stalloid.

intravascular fluidvolume.

Expansion ofplasmavolume andmaintenanceof cardiacoutput inf i o o u w

drug given alone,

=Pain: Assess type, location,and intensity prior to and 30-60min following administration.

(diaphoresis, tachycardia, &malaise).=Monitor vi.tal signs, CVP, andintake and output before andfrequently throughout therapy.If fever, tachycardia, orhypotension occurs, stopinfusion and notify physician~~!!DHypotension may also resultfrom infusing too rapidly. Maybe given without regard topatient's blood group.

with fluidvolume deficit,includingshock,hemorrhage,and burns.Temporary =Assess for signs of vascularreplacement of overload (elevated CVP,

@ l l i 1 O

@ l l i 1 O

"Thera peutic:volume expanders

=Pharmacologic:

with lowlevels ofplasmaproteins, suchas nephroticsyndrome orend-stage liverdisease,

administration.

~~m~f U @ ~ ~ Q l ] ~ [ f U ~ Dassociated -edema.

@ l l i 1 O


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Table 1Algorithm for the virological diagnosis of Dengue~ ~ D ~ D U Q O ~ ~ D D U @ ~ ~ Q O ~ D U ~ D @ @ U

Outbreak mode Clinical Specimen Time of collection Storage - Shipment Test of Delay for report(')Diagnosis Choice

Virus isolation2-4 weeks

evaluationmodes

Serum After 1 week after then store at RT-PCR 2-7 days

Monitoringmode

DF

Always, DHF/OSS Serum Less than 4 days Let blood S hip o n ice~ ~ D ~ D U Q O ~ ~ ~ I D ~ ~ Q O ~ D U s ~ ~ ~ @ q" : ~ k f t e ' : : ~ : : : : : tat 4C) Virus isolation2-4 weeksRT-PCR 2-7 daysth e outbreak onset

Serum ~ I T I Q O ~ ~ D D U @ ~ ~ Q O ~ ~ ~ o l ~ @ t i W t ~ ~ : ~ ~Otherwise the laboratwait for2nd serum


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~~~lli)[ill~@~~~8@J@{mGB@[]UU-ime of collection Storage Shipment Test of Delay for repgC:!Jij'1:llagnOSls Choice

Post-mortem Heart blood, As soon as Insterile IgM Elisa 1-7daysliver, kidney or possible after container

Virus isolation2-4 weeks

RT-PCR 2-7 days

~ ~ ~ ~ [ j j )Q ! ]~ ~ ~ [ j j )@ ~ ~ Q ! ]~ [ j j ) ~ D @ @ U ilU

~ ~ ~ ~ [ j j )Q ! ]~ ~ ~ [ j j ) @ ~ ~ Q ! ] ~ [ j j ) ~ D @ @ U i l U

~ ~ ~ ~ [ j j )Q ! ]~ ~ ~ [ j j )@ ~ ~ Q ! ]~ [ j j ) ~ D @ @ U ilU


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Table 2Interpretation of test results

Type of test

Virus isolation and typing Serum taken less than 4 Conf irms etiology and ident if ies the Does not rule out Dengue indays after onset Dengue virus type The rate of false negatives

depends mainly onthe condiof shipment~ ~ ~[ f i] ( il l~ ~ ~[ f i]@ ~ ~ ( il l~ [ f i] ~ D @ l l i lU

RT-PCR (reversetranscriptase-polymerase

Under investigation. The genimpression is that under rout

chain reaction)

IgM ELISA

conditions itwil l yield less falS e r u m. ~ ~ ~ ~ . ~ ~ ~ ~ , ~ ~ @ . ~ o ~week of onset Flavivirus (*) sera taken very close to the

of the disease ( 00 )

1 n J ~ ~ ~ [ f i ]( i l l~ ~ ~ [ f i] ( Q l~ ! I ~ I n l ~ ~~tak," withinl? t0~Qj~~~A-b W~IJ~~after onset Single serum: Titer >/= 1280 Single serum: t ited "" 1280Suggestive of secondary infection Not informat ivePaired sera: 1st serum Paired sera: 4-fold increase in titer Paired sera: less than 4-fold

after the 1st .


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NORMAL VALUE SIGNIFICANCE

Hematocrit (Hct)White blood cell (WBC) count

35% - 45%

Differential WEe count 4.5 - 13.5 xl03 C ~ I @ l l l i J( i l l~

3 - 5.8 X 103cel~mrn30.05 - 0.25 x 103 cells/mm"

NeutrophilsEosinophils

RESULT

-4.2-11.1-34%-13x 103~ l l i J ~ @ U Q D ~ U O ~ D I T D O-4.3-0.15-0.022-3.2 X 103-5.1%

Platelet count


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The vectors of DHF breed inand around houses and, in principle, can be controlled by individualand community action. nus approach should b ~ \ i t : ~ n dn exten"il'g vectorcommunities that do not routinely benefit from th~~[lJ~@~@@disease is transmitted by Aedes mosquito. For practical purposes it may be assumed that the vector isA ede s a eg yp ti, a mosquito that bites during the day, rests in houses and lays eggs in artificial water

collect water such as old tires, empty tins and bottles and broken jars, and by routinely changing thewater in flower vases once a week. Whenever po~Rfl~l1rITdf\!"\~~~m~u1f;:0@~side down before refilling with water. Water ja~UillillWll~U~~~~~JJ~~~ a lllllladequately covered to prevent egg-laying by A e de s a eg y pt i, or clean and scrub weekly. When this is notpossible owing to their shape and size, Aedes larvae should be eliminated by transferring the water from

In certain areas where vectors other than A e de s a eg y pt i are present, coconut shells and husks canbe buried or burned, tree holes can be filled with sand~.ore~ffrt, leaf axils tfn be.puni\red ;tI~h~Asof bamboo fences altered to prevent accumulation . m J W Q B W @ H [ID ~ ~ u l ! l~ ~ ~ @ @without a piped water supply, large water tanks witl taps should be covered sotU to allow rainwater toenter but exclude egg-laying mosquitoes.

n n rr;] n n r?~rrR~~~mwtf~~at~e~ucation should be provided regularly, beginning atlJUuULYJ1JJhl~~~~lliJ~UM~i3~J.rMJUtUple but accurate mformation and usmg all available

media/school books, lectures, newspapers, radio and pamphlets. While health education should aim tocover the whole population, more specific efforts should be directed towards providing information forkey components of the communication, such as p O O o o 8 m ~ ~ ~ @ @ ~ ~ d @ @ l l i i l leducation should cover vector-borne disease in gWe~~ ~ith special em~~at;U on DHF wherever thisconstitutes a major problem.


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Dengue haemorrhagic fever: diagnosis, treatment and control. Geneva: World Health Organization;1986Mackenzie, John S. Viral Diseases in South-E~_~~@ffiJ~D@[Jili)Press; 1982 W ~T IU U \:VUUU~Shryock, Harold. Modern Medical Guide. Philippines: Philippine Publishing House; 1981

Huether, Sue E. and McCance, Kathryn L. Understanding Pathophysiology. Singapore: Elsevier 2004ractice, 2nd edition. Philadelphia: F.A. Davis Co.;

2006 UU~\:V

Lennette, Edwin H. Laboratory Diagnosis of Viral Infections. New York: Marcel Dekker, Inc.; 1985: ~ a : ~ : : , ' : : : : , ~ : " ; : : : : : , : ' ~ ~ : : t i '1 l l i r n r ~ Q ! ] ~ ~ r ~ @ n ~ ~ ~ @ r m D @Whaley and Wong. Nursing Care of Infants and Children, Vol. II, 3rd edition. Toronto: C.V. Mosby

Co.; 1987~ D n HO.Cl4flnbem .,M~Wnn)JlE~~~ of Pediatric Nursing, 7th edition. Singapore: Elsevier Inc.; 2005~ U U ~ u l l i l~_~~~~~~s Pocket Guide, 9th edition. Philadelphia: F.A.

Davis Co.; 2004 Microsoft Encarta 2006


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Dengue hemorrhagic fever (DHF) iSI@)OO~~~@~OO~t1l]~@ffiJ~a@@ITili)Residing in an urban region in the [philiPPines, which i~~~arentIY a riskarea, has made me well-acquainted with the prevalence of such illness.

~~~~~f~~~@~rr~~~~D@UuDroved to be insufficient and limited.The creation of this case presentation enabled me to study and understandthe nature and complexities of Dengue hemorrhagic fever in a scientific,comprehensive, yet appreciative man~._!ID(il1M~D'@@ITili)society, it will truly be of great use and help to be k~ledgeable aboutdiseases that are infectious and threatening to health, such as DHF.

~DnT~eoret.iq~1co.nce91;s,~.dies~n~~~ics are very esse.ntial towards a care~ U U ~ l i l l M ~ ~ B ~ O O @ ~ 8 f l l r u @ ~ ~ patients, because these are strongfoundations that will guide the practical aspect of care giving.

This case presentation was indeed an ~M~~~Iffi~D@ITili)my future endeavors as a nurse, and e!fe~~s an individual.

Nursing Case Study Dhf Dengue Hemorrhagic Fever

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