casestudy dengue

1 Case Study: dengue fever

OBJECTIVES

General:This case presentation aims to identify and determine the

general health problems and needs of the patient with an admitting diagnosis of Dengue Fever. This study also intends to help promote health and medical understanding of such condition through the application of the nursing skills.

Specific: To enhance knowledge and acquire more information about

Dengue Fever To give an idea of how to render proper nursing care for

clients with this condition thus it can be applied for future exposures of students

To gather the needed data that can help to understand how and why the disease occurs

To identify laboratory and diagnostic studies used in Dengue Fever

To enumerate the clinical manifestations of the disease so as to provide prompt intervention of its occurrence


ACKNOWLEDGEMENT

First and foremost, I would like to express my sincerest gratitude to our Almighty God for giving me the ability and chance to finish this study and for guiding me in my everyday life and activities.

I also wish to express my deepest gratitude to my family for providing me everything I need and for their untiring support.

I also thank my friends for their constant encouragement.

And to the patient and his mother, I want to extend my gratitude for their cooperation and for giving me the information I need to finish this requirement.

It is also my pleasure to thank the Dean of College of Nursing, Dean May Veridiano for being always considerate and approachable and for establishing a good quality of education in our department. And to all our instructors/faculty members, I thank them for their guidance and all the knowledge, discipline, and lessons they have shared to us.

Finally, I thank my most beloved teachers and those special people who made me feel that they believe in me more than I do to myself.


INTRODUCTION:Background of the

Disease


Dengue Virus Infection And Dengue Hemorrhagic Fever

DefinitionDengue fever and dengue hemorrhagic fever (DHF) are acute febrile diseases

which occur in the tropics, can be life-threatening. It occurs in tropical and sub-tropical areas of the world. Dengue fever is a febrile illness that affects infants, young children and adults.

Dengue is a mosquito-borne infection that in recent decades has become a major international public health concern.

Dengue fever syndrome is the type of dengue without significant hemorrhages.Dengue hemorrhagic fever is a severe, potentially deadly infection with gross

hemorrhages spread by certain species of mosquitoes.

Other NamesHemorrhagic Fever or H-fever, Acute Infectious Thrombocytopenic Purpura, Dengue Shock Syndrome, Breakbone Fever, Bonecrusher Disease, Dandy Fever, Philippine/Thai/Singapore Hemorrhagic Fever

Etiologic Agent four closely related virus serotypes of the genus Flavivirus, family Flaviviridae

(Dengue Virus I,II,III,IV) three other arboviruses (Chikungunya, O’nyong-nyong and West Nile Fever,

have been identified with dengue-like diseases

Mode of Transmission

http://en.wikipedia.org/wiki/Flaviviridae

http://en.wikipedia.org/wiki/Flavivirus

http://en.wikipedia.org/wiki/Serotype

http://en.wikipedia.org/wiki/Virus

http://en.wikipedia.org/wiki/Tropics

http://en.wikipedia.org/wiki/Tropical_disease

http://en.wikipedia.org/wiki/Fever


Dengue viruses are transmitted to humans through the bites of infective female Aedes mosquitoes. Mosquitoes generally acquire the virus while feeding on the blood of an infected person. After virus incubation for eight to 10 days, an infected mosquito is capable, during probing and blood feeding, of transmitting the virus for the rest of its life. Infected female mosquitoes may also transmit the virus to their offspring by transovarial (via the eggs) transmission

Incubation PeriodThe incubation period of Dengue fever is usually 5 to 6 days but may vary from 3

to 10 days.

Portal of EntrySkin

Period of CommunicabilityInfected person with Dengue becomes infective to mosquitoes 6 to 12 hours

before the onset of the disease and remains up to 3 to 5 days.The mosquito becomes infective from day 8-12 after the blood meal and remains

infective throughout life.

Pathology- generalized vasculitis and effusion in serous cavities are important postmortem

findings among those who die in shock without evidence of gross hemorrhages.- In frank hemorrhagic cases the upper GIT may show hemorrhages- There is subcapsular hemorrhage of the liver with fatty metamorphosis or focal

coagulation necrosis- There are occasional basophilic and acidophilic cells with cytoplasmic

vacuolation in the sinusoids- There is proliferation of Kuffer cells with lymphocytic infiltration and plasma cells

around the portal area.- The lungs show marked congestion with focal hemorrhages and blood may fill up

the alveolar spaces.- The adrenals show stimulation of the zona fasciculate and zona reticularis do not

show much change; these findings are interpreted as a response to stress.- Enlarged and prominent lymphoid follicles in the ileum, Peyer’s patches, and

mesenteric lymph nodes are described.- In the bone marrow, maturational arrest of megakaryocytes is observed. - In the different organs, perivascular edema and diapedesis of red blood cells are

noted.- Immunoflourescent direct staining allows the identification and localization of

dengue antigen in the tissues of fatal cases.

Pathognomonic sign


Herman’s sign - is classically a widespread erythema with small white patches of edema 'in a sea of red'

Clinical ManifestationsThe disease manifests as a sudden onset of severe headache, muscle and joint

pains (myalgias and arthralgias—severe pain that gives it the nickname break-bone fever or bonecrusher disease), fever, and rash. The dengue rash is characteristically bright red petechiae and usually appears first on the lower limbs and the chest; in some patients, it spreads to cover most of the body. There may also be gastritis with some combination of associated abdominal pain, nausea, vomiting, or diarrhea.

Some cases develop much milder symptoms which can be misdiagnosed as influenza or other viral infection when no rash is present. Thus travelers from tropical areas may pass on dengue inadvertently, having not been properly diagnosed at the height of their illness. Patients with dengue can pass on the infection only through mosquitoes or blood products and only while they are still febrile. The classic dengue fever lasts about two to seven days, with a smaller peak of fever at the trailing end of the disease (the so-called "biphasic pattern"). Clinically, the platelet count will drop until the patient's temperature is normal. Cases of DHF also show higher fever, variable hemorrhagic phenomena, thrombocytopenia, and hemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate.

DENGUE FEVER Abrupt onset of high fever Severe frontal headache Pain behind the eyes(retero-orbital pain) which worsens with eye movement Muscle and joint pains Loss of sense of taste and appetite Measles-like rash over chest and upper limbs Nausea and vomiting Minor hemorrhagic manifestations like petechiae, bleeding from nose or gums

may occur. Lymphadenopathy with leukopenia and relative lymphocytosis are common.

Thrombocytopenia(platelet count £ 100x103) and raised transaminases occur less frequently.

DENGUE HAEMORRHAGIC FEVER AND DENGUE SHOCK SYNDROME Symptoms similar to dengue fever. Or history of recent fever. Illness is often

biphasic beginning with fever with symptoms as in dengue. During recovery phase of fever patient’s condition worsens markedly with severe weakness, marked restlessness, facial pallor and often diaphoresis and circumoral cyanosis, severe continuous pain abdomen. Liver may be enlarged. Thrombocytopenia ( platelet count £ 100x103 ) also occurs during this phase.

Haemmorhagic phenomenon are frequent and include positive tourniquet test, petechae, easy bruising, bleeding from venepuncture sites, epistaxis, bleeding from mouth & gums and skin rashes.

http://en.wikipedia.org/wiki/Dengue_shock_syndrome

http://en.wikipedia.org/w/index.php?title=Hemoconcentration&action=edit&redlink=1

http://en.wikipedia.org/wiki/Thrombocytopenia

http://en.wikipedia.org/wiki/Platelet


http://en.wikipedia.org/wiki/Influenza

http://en.wikipedia.org/wiki/Diarrhea

http://en.wikipedia.org/wiki/Vomiting

http://en.wikipedia.org/wiki/Nausea

http://en.wikipedia.org/wiki/Abdominal_pain

http://en.wikipedia.org/wiki/Gastritis

http://en.wikipedia.org/wiki/Petechiae

http://en.wikipedia.org/wiki/Rash


http://en.wikipedia.org/wiki/Arthralgia

http://en.wikipedia.org/wiki/Myalgia


Frequent vomiting with or without blood. Bleeding from GI tract is an ominous sign that usually follows a prolonged period of shock. There may be signs of plasma leakage indicated by small pleural effusion or ascites. Hepatomegaly is common but is not accompanied by jaundice.

Patient may go into shock manifested by :Pale, cold or clammy skin,sleepiness and restlessness,patient feels thirsty and mouth becomes dry,rapid weak pulse and difficulty in breathing.

Complications Encephalopathy Liver damage Residual brain damage Seizures Shock

CASE DEFINITIONS DENGUE FEVER: Suspect case: Acute onset and high fever of 2-7 days duration, and two or more of the following:Headache,retero-orbital pain, myalgia, arthralgia, rash, hemorrhagic manifestations, and leucopenia. Probable case: Suspect case and one or more of the following: Occurance of confirmed cases of dengue in the same place and time. Detection of IgM antibody. IgM antibody indicates current or recent infection and is detectable 6-7 days after onset of illness. If available Mc- Elisa test is more specific. Confirmed case: Suspect or probable case and one or more of the following:Isolation of virus or detection of viral genomic sequences. fourfold rise in titres of IgG or IgM antibody. For this at least 2 samples are to be taken- one at the time at the time of reporting to a clinic or a hospital and second shortly before discharge . The optimum interval between two samples should be 10 days. Although serological tests are simpler, they can give false positive results due to cross reaction between antibodies against dengue and other flaviviruses. Confirmatory tests are not necessary for management of cases and should be done to confirm the aetiology of the outbreak.

DENGUE HAEMMORHAGIC FEVER Probable or confirmed case of dengue, and Haemorrhagic tendencies as described under DHF. Thrombocytopenia(platelet count £ 100x103 ).Evidence of plasma leakage

due to increased vascular permeability, manifested one or more of the following: a rise in average haematocrit for age and sex ³20%, a ³20% drop in haematocrit following volume replacement compared to baseline, signs of plasma leakage indicated by pleural effusion or ascites ( demonstrated by ultrasonography or x-ray), hypoproteinemia. Slight elevation of liver enzymes, hypoproteinemia and low levels of C 3 complement proteins are commonly observed. Prothrombin, partial


thromboplastin, thrombin times may be prolonged in many cases. While a normal WBC count or leukopenia with neutrophils predominating is common initially, a relative lymphocytosis with more than 15% atypical lymphocytes is common when fever subsides.

DENGUE SHOCK SYNDROME All the criteria for DHF Evidence of circulatory failure as detailed under DSS

Classification

o Severe, frank typeWith flushing, sudden high fever, severe hemorrhage, followed by sudden drop of temperature, shock and terminating in recovery or death.

o ModerateWith high fever, but less hemorrhage, no shock

o MildWith slight fever, with or without petechial hemorrhage but epidemiologically related to typical cases usually discovered in the course of investigation of typical cases.

DiagnosisA physical examination may reveal:

Enlarged liver (hepatomegaly) Low blood pressure Rash Red eyes Red throat Swollen glands Weak, rapid pulse

Tests may include: Arterial blood gases Coagulation studies Electrolytes Hematocrit Liver enzymes Platelet count Serologic studies (demonstrate antibodies to Dengue viruses) Serum studies from samples taken during acute illness and convalescence

(increase in titer to Dengue antigen)

http://www.nlm.nih.gov/medlineplus/ency/article/002224.htm









Tourniquet test/Rumpel Leads Test (causes petechiae to form below the tourniquet)

X-ray of the chest (may demonstrate pleural effusion)

Nursing ManagementAny disease or condition associated with hemorrhage is enough cause for alarm.

Immediate control of hemorrhage and close observation of the patient for vital signs leading to shock are the nurse’s primary concern. Nursing measures are directed towards the symptoms as they occur but immediate medical attention must be sought:

For Hemorrhage- Keep the patient at rest during bleeding episodes.- For nose bleeding, maintain an elevated position of trunk and promote

vasoconstriction in nasal mucosa membrane through an ice bag over the forehead.

- For melena, ice bag over the abdomen.- Avoid unnecessary movement- If transfusion is given, support the patient during the therapy.- Observe signs of deterioration(shock) such as low pulse, cold clammy

perspiration, prostration. For Shock

- Prevention is the best treatment- Dorsal recumbent position facilitates circulation- Adequate preparation of the patient, mentally and physically prevents

accurrence of shock.- Provision of warmth through lightweight covers (overheating causes

vasodilation which aggravates bleeding) Diet

- Low fat, low fiber, non-irritating, non-carbonated- Noodle soup may be given

For Fever- Cooling measures(tepid sponge bath)- Administer prescribed drugs- Encourage fluid intake unless contraindicated

PrognosisWith early and aggressive care, most patients recover from dengue hemorrhagic

fever. However, half of untreated patients who go into shock do not survive.


10

Case Study: dengue fever

DEFINITION OF TERMS Tropics – hot and humid places Anaphylactoid - a rapidly progressing, life-threatening

allergic reaction DIC – (Disseminated Intravascular Coagulation) also known

as consumptive coagulopathy, is a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases

Prothrombin – a plasma protein that is converted into thrombin during blood clotting

Thromboplastin - any of a group of substances that are liberated from damaged blood platelets and other tissues and convert prothrombin to thrombin Also called thrombokinase

Fibrinogenopenia - decrease in concentration of fibrinogen in the blood.

Megakaryocytes – a large bone marrow cell with a lobulate nucleus that gives rise to blood platelets. Also called megalokaryocyte.

Diapedesis – the movement or passage of blood cells, especially white blood cells, through intact capillary walls into surrounding body tissue.

Herman’s sign – is classically a widespread erythema with small white patches of edema 'in a sea of red'

Petechiae – are small (1-2mm) red or purple spot on the body, caused by a minor hemorrhage (broken capillary blood vessels)

Hemoconcentration – a decrease in plasma volume resulting in an increase in the concentration of red blood cells in blood.

http://en.wikipedia.org/wiki/Blood_vessel

http://en.wikipedia.org/wiki/Blood_vessel

http://en.wikipedia.org/wiki/Capillary

http://en.wikipedia.org/wiki/Hemorrhage

http://en.wikipedia.org/wiki/Coagulation

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Lymphocytosis - is an increase in the number or proportion of lymphocytes in the blood, usually detected when a complete blood count is routinely obtained.

SOURCE: www.google.com

Personal Background of the

Patient

http://en.wikipedia.org/wiki/Complete_blood_count

http://en.wikipedia.org/wiki/Lymphocyte

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PERSONAL DATAName: Patient X

Address: Arayat St. Nagkaisang Nayon, Quezon City

Occupation: none (student)

Religion: Roman Catholic

Nationality: Filipino

DEMOGRAPHIC DATADate of Birth: December 14,1996

Place of Birth: Manila

Age: 13 years old

Gender: Male

Civil Status: Single

PATIENT PROFILEDate Admitted: May 15, 2010

12:43 pm

Attending Physician: Dr. Dominador D Wayet

Room/Ward: Pavilion III

Hospital Record No: 495501

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HOME ENVIRONMENT AND OCCUPATION

Physical Environment: He is studying in a public school and he is

living with his parents and other siblings and

their families. His parents have no occupation.

His 4 older siblings support their family needs.

He doesn’t smoke or drink alcoholic

beverages.

NUTRITIONAL PATTERN

Usual Meal: He usually eats fried foods and seldom eats

vegetables. And he usually drinks 6 glasses of

water every day.

SLEEP AND REST PATTERN

Usual Sleep Pattern: Usually sleeps at 9 or 10 o’clock in the

evening and wakes up at 6:30 in the morning.

But during hospitalization, he frequently sleep

even on daytime.

Relaxation Techniques: Internet surfing, video games and watching

television are his relaxation techniques.

ELIMINATION PATTERN

Urinary: He urinates 3-4 times a day

Bowel: He defecates once a day.

PAST HEALTH HISTORY

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Past Medical History

In the year 2000, he was diagnosed with primary complex and had

taken medicines (unrecalled) for six months.

He had three previous history of dog bites in the year 2001, 2002 and

2004. He had his rabies vaccines on 2001.

Medications

Paracetamol (Biogesic)

Robitusin

Vaccinations

OPV (3)

BCG (1)

DPT (3)

Measles (1)

HepaB (3) = ?unsure

Allergies

No known allergies to food and drugs

Family History

Pulmonary Tuberculosis: grandfather(paternal), father

Hypertension: mother, father, siblings

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HISTORY OF PRESENT ILLNESS

Reason for seeking medical care: Persisting on and off Febrile episodes

One week prior to admission, the patient had a night swimming with his friends. He slept on the seashore and had a fever the next morning.

Four days PTC, the patient also experienced abdominal pain, loose bowel movement(2x), vomiting approximately 1cup/about every after feeding. He had self medication of Paracetamol 500mg BID.

Two days PTC, patient still has intermittent fever.Upon admission, vomiting and diarrhea were still present on the first

two days. D5 0.3NaCl @ KVO rate upon admission D5 0.3NaCl x 8° (5/16/10) D5 LR 1L (5/17/10)

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PHYSICAL EXAMINATION

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Vital SignsUpon Admission Latest

Temperature 38.1°C 36.5°CPulse 80beats/min 76beats/minRespiration 38breaths/min 29breaths/minBlood Pressure 110/60mmHg 90/60mmHg

HEIGHT: 166cmWEIGHT: 42kg

GENERAL No weight loss noted Less energy to conduct usual activities

HEADSkull and Face

Rounded, normocephalic and symmetrical Uniform consistency; absence of nodules or masses Symmetric facial movements No tenderness Can move facial muscles at will

SCALP Dry Free from lice and nits No tenderness nor masses Same color as the complexion No lesions

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SKIN The skin color is normal No petechial rashes No skin abrasions or lesions No edema present Dry skin Temperature is within normal range No itchiness

HAIR Evenly distributed hair Black Variable amount of body hair

NAILS Convex curvature Smooth in texture With capillary refill of 2-3 seconds

Eyes,Eyebrows and Eyelashes Eyebrows symmetrically aligned Equally distributed eyelashes Skin intact ; no discharges Anecteric Sclera Pink palpebral conjunctiva No edema or tenderness present over lacrimal gland No eyeglasses

Ears Auricle symmetrical, aligned with outer canthus of the eyes Mobile, firm and not tender,; pinna recoils after it is folded Normal voice tones audible No discharges

Nose and Sinuses

External nose is symmetric and straight Clear-watery discharge and flaring of the nares Uniform in color

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No tenderness or lesions when palpated Airway is patent (air moves freely as the client breathes through

the nares) Nasal septum intact and in midline

Mouth and Oropharynx

Outer lips is dry Tongue in central position, pink in color; with raised papillae;

moves freely

NECK Neck muscles equal in size, head is centered Coordinated, smooth movements without discomfort No enlarged lymph nodes

THORAX AND LUNGS With frequent coughs and colds Chest symmetric Chest wall intact; no tenderness, no masses Not in respiratory distress No retractions

CARDIOVASCULAR With palpitations No chest pain No shortness of breath Adynamic precordium No murmurs

GASTROINTESTINAL Soft,nontender abdomen No dysphagia Vomiting and diarrhea were present few days before admission

and first 2 days upon admission Normoactive bowel sounds

MUSCULOSKELETAL SYTEM Equal in size on both sides of body No contractures; no tremors

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Coordinated movements Malaise/weakness Thin extremities Decreased Activity Tolerance No muscle pains or joint swelling

EXTREMITIES No edema Symmetric With full and equal pulses

Laboratory Examinations

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Hematology(5/15)

Result Normal values

Interpretation

WBC 1.7 4.8-10.8x109/L

Decreased: some medications, some

autoimmune conditions, some severe infections, bone

marrow failure, and congenital marrow aplasia

RBC 5.50 4.7-6.1x1012/L Within normal rangeHgb 14.81 13-17g/L Within normal rangeHct 44.27 40-52% Within normal range

MCV 81 82-98fl Decreased: microcytic anemia

MCH 26.94 28-33pg Decreased: decreased with iron deficiency and

thalassemiaMCHC 33 33-36g/L Within normal range

Platelets 51 150-400x109/L

Decreased:thrombocytopenic purpura,acute leukemia,

aplastic anemia,and during cancer chemotherapy

Neutrophils 39.50 40-70% Decreased: viral infections, bone marrow,suppression,

primary bone marrow sadisease

Lymphocytes 45.50 19-48% Within normal range

http://www.labtestsonline.org/understanding/conditions/thalassemia.html

http://www.labtestsonline.org/glossary/congenital.html

http://www.labtestsonline.org/understanding/conditions/autoimmune.html

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Monocytes 8.90 2-8% Increased: viral infections,parasitic disease, collagen

and hemolytic disordersEosinophils 1.80 3-9% Decreased: stress, use of

some medications(ACTH, epinephrine, thyroxine)

Basophils 4.30 0-5% Within normal rangeBlood type O

Hematology(5/16)


Interpretation

WBC 2.8 4.8-10.8x109/L



marrow failure, and congenital marrow aplasia

RBC 5.08 4.7-6.1x1012/L

Within normal range

Hgb 13.78 13-17g/L Within normal rangeHct 41.62 40-52% Within normal range

MCV 82 82-98fl Within normal rangeMCH 27.14 28-33pg Decreased: iron deficiency

and thalassemiaMCHC 33 33-36g/L Within normal range

Platelets 36 150-400x109/L

Decreased:thrombocytopenic purpura,acute leukemia,

aplastic anemia,and during cancer chemotherapy

Neutrophils 34.40 40-70% Decreased: viral infections, bone marrow

suppression, primary bone marrowdisease

Lymphocytes 58.80 19-48% Increased: infectiousmononucleosis, viral and some bacterial infections,




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hepatitisMonocytes 1.80 2-8% Decreased: use of

corticosteroids, RA, HIVinfection

Eosinophils 0.70 3-9% Decreased: stress, use of some medications(ACTH, epinephrine, thyroxine)

Basophils 4.30 0-5% Within normal range

Hematology(5/17)


Interpretation

WBC 2.2 4.8-10.8x109/L



marrow failure, and congenital marrow aplasiab

RBC 5.28 4.7-6.1x1012/L

Within normal range

Hgb 14.42 13-17g/L Within normal rangeHct 43.37 40-52% Within normal range

MCV 82 82-98fl Within normal rangeMCH 27.33 28-33pg Decreased: decreased with

iron deficiency and thalassemia

MCHC 33 33-36g/L Within normal rangePlatelets 20 150-

400x109/LDecreased:thrombocytopenic

purpura,acute leukemia,aplastic anemia,and during

cancer chemotherapyNeutrophils 28.10 40-70% Decreased: viral infections,

bone marrow suppression, primary bone marrowdisease

Lymphocytes 55.50 19-48% Increased: infectiousmononucleosis, viral and some bacterial infections,




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hepatitisMonocytes 8.0 2-8% Within normal rangeEosinophils 4.30 3-9% Within normal rangeBasophils 4.10 0-5% Within normal range

Urinalysis


Interpretation

Color Yellow Lt. yellow-Amber

Normal

Transparency Hazy Clear Semen, mucus, and lipid may cause

turbidity.Increased numbers of cells, crystals,

casts, or organisms can increase the turbidity of

urine in disease conditions.

Sp.Gravity 1.020 1.015-1.030 NormalReaction 6.5 ph 4.8-7.7 Within the Normal Range

Sugar (-) (-) NormalProtein +2 (-) Nephritis,Cardiac

failure,Mercury poisoning,Bence-Jones

protein in multiple myeloma

Febrile states HematuriaRBC 0-1 0-2/hpf Within the Normal RangeWBC 0-1 0-5/hpf Within the Normal Range

Epith.cells Few Few/present NormalCrystals Few A.urates-few Normal

M. Threads Moderate Few/present mucosal surface irritations

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Urobilinogen +1 1.20 NormalNitrate (-) (-) NormalBlood (-) (-) Normal

Bilirubin (-) (-) NormalKetone (-) (-) Normal

Leukocyte (-) (-) Normal

Anatomy and Physiology

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Circulatory System

The circulatory system is made up of the vessels and the muscles that help and control the flow of the blood around the body. This process is called circulation. The main parts of the system are the heart, arteries, capillaries and veins.

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Blood is a specialized bodily fluid that delivers necessary substances to the body's cells – such as nutrients and oxygen – and transports waste products away from those same cells.

Red blood cells – also called erythrocytes, are biconcave discs, which means their centers are thinner than their edges. These are the only human cells without

http://en.wikipedia.org/wiki/Waste

http://en.wikipedia.org/wiki/Oxygen

http://en.wikipedia.org/wiki/Cell_(biology)

http://en.wikipedia.org/wiki/Body_fluid

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nuclei. They contain the protein hemoglobin, which gives them the ability to carry oxygen.

White blood cells – also called leukocytes, are larger than RBCs and have nuclei when mature. There are five kinds of WBCs: neutrophils, eosinophils, basophils, lymphocytes and monocytes. They all contribute to the same general function, which is to protect the body from infectious disease and to provide immunity to certain diseases.

Platelets – more formally known as thrombocytes, which are not whole cells but rather fragments or pieces of cells. They are necessary for hemostasis, which means prevention of blood loss.

ARTERIES

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Arteries carry blood from the heart to capillaries; smaller arteries are called arterioles. If we look at an artery in cross-section, we find three layers (or tunics) of tissues, each with different functions (Fig. 13–1). The innermost layer, the tunica intima, is the only part of a vessel that is in contact with blood. It is made of simple squamous epithelium called endothelium. This lining is the same type of tissue that forms the endocardium, the lining of the chambers of the heart. As you might guess, its function is also the same: Its extreme smoothness prevents abnormal blood clotting. The endothelium of vessels, however, also produces nitric oxide (NO), which is a vasodilator. The tunica media, or middle layer, is made of smooth muscle and elastic connective tissue. Both of these tissues are involved in the maintenance of normal blood pressure, especially diastolic blood pressure when the heart is relaxed. The smooth muscle is the tissue affected by the vasodilator NO; relaxation of this muscle tissue brings about dilation of the vessel. Smooth muscle also has a nerve supply; sympathetic nerve impulses bring about vasoconstriction. Fibrous connective tissue forms the outer layer, the tunica externa. This tissue is very strong, which is important to prevent the rupture or bursting of the larger arteries that carry blood under high pressure. The outer and middle layers of large arteries are quite thick. In the smallest arterioles, only individual smooth muscle cells encircle the tunica intima. As mentioned, the smooth muscle layer enables arteries to constrict or dilate. Such changes in diameter are regulated by the medulla and autonomic nervous system, and will be discussed in a later section on blood pressure. VEINS

Veins carry blood from capillaries back to the heart; the smaller veins are called venules. The same three tissue layers are present in veins as in the walls of arteries, but there are some differences when compared to the arterial layers. The inner layer of veins is smooth endothelium, but at intervals this lining is folded to form valves. Valves prevent backflow of

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blood and are most numerous in veins of the legs, where blood must often return to the heart against the force of gravity. The middle layer of veins is a thin layer of smooth muscle. It is thin because veins do not regulate blood pressure and blood flow into capillaries as arteries do. Veins can constrict extensively, however, and this function becomes very important in certain situations such as severe hemorrhage. The outer layer of veins is also thin; not as much fibrous connective tissue is necessary because blood pressure in veins is very low.

ANASTOMOSES

An anastomosis is a connection, or joining, of vessels, that is, artery to artery or vein to vein. The general purpose of these connections is to provide alternate pathways for the flow of blood if one vessel becomes obstructed. An arterial anastomosis helps ensure that blood will get to the capillaries of an organ to deliver oxygen and nutrients and to remove waste products. There are arterial anastomoses, for example, between some of the coronary arteries that supply blood to the myocardium. A venous anastomosis helps ensure that blood will be able to return to the heart in order to be pumped again. Venous anastomoses are most numerous among the veins of the legs, where the possibility of obstruction increases as a person gets older.

CAPILLARIES

Capillaries carry blood from arterioles to venules. Their walls are only one cell in thickness; capillaries are actually the extension of the endothelium, the simple squamous lining, of arteries and veins. Some tissues do not have capillaries; these are the epidermis, cartilage, and the lens and cornea of the eye. Most tissues, however, have extensive capillary networks. The quantity or volume of capillary networks in an organ reflects the metabolic activity of the organ. The functioning of the kidneys, for example, depends upon a good blood supply. In contrast, a tendon such as the Achilles tendon at the heel or the patellar tendon at the knee would have far fewer vessels, because fibrous connective tissue is far less metabolically active. Blood flow into capillary networks is regulated by smooth muscle cells called precapillary sphincters, found at the beginning of each network. Precapillary sphincters are not regulated by the nervous system but rather constrict or dilate depending on the needs of the

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tissues. Because there is not enough blood in the body to fill all of the capillaries at once, precapillary sphincters are usually slightly constricted. In an active tissue that requires more oxygen, such as exercising muscle, the precapillary sphincters dilate to increase blood flow. These automatic responses ensure that blood, the volume of which is constant, will circulate where it is needed most. Some organs have another type of capillary called sinusoids, which are larger and more permeable than are other capillaries. The permeability of sinusoids permits large substances such as proteins and blood cells to enter or leave the blood. Sinusoids are found in the red bone marrow and spleen, where blood cells enter or leave the blood, and in organs such as the liver and pituitary gland, which produce and secrete proteins into the blood

EXCHANGE IN CAPILLARIES

Capillaries are the sites of exchanges of materials between the blood and the tissue fluid surrounding cells. Some of these substances move from the blood to tissue fluid, and others move from tissue fluid to the blood.

Gases move by diffusion, that is, from their area of greater concentration to their area of lesser concentration. Oxygen, therefore, diffuses from the blood in systemic capillaries to the tissue fluid, and carbon dioxide diffuses from tissue

fluid to the blood to be brought to the lungs and exhaled.Let us now look at the blood pressure as blood enters capillaries from

the arterioles. Blood pressure here is about 30 to 35 mmHg, and the pressure of the surrounding tissue fluid is much lower, about 2 mmHg. Because the capillary blood pressure is higher, the process of filtration occurs, which forces plasma and dissolved nutrients out of the capillaries and into tissue fluid. This is how nutrients such as glucose, amino acids, and vitamins are brought to cells.

Blood pressure decreases as blood reaches the venous end of capillaries, but notice that proteins such as albumin have remained in the

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blood. Albumin contributes to the colloid osmotic pressure (COP) of blood; this is an “attracting” pressure, a “pulling” rather than a “pushing” pressure. At the venous end of capillaries, the presence of albumin in the blood pulls tissue fluid into the capillaries, which also brings into the blood the waste products produced by cells. The tissue fluid that returns to the blood also helps maintain normal blood volume and blood pressure.

PATHWAYS OF CIRCULATION

The two major pathways of circulation are pulmonary and systemic. Pulmonary circulation begins at the right ventricle, and systemic circulation begins at the left ventricle. Hepatic portal circulation is a special segment of systemic circulation that will be covered separately. Fetal circulation involves pathways that are present only before birth and will also be discussed separately.

PULMONARY CIRCULATION

The right ventricle pumps blood into the pulmonary artery (or trunk), which divides into the right and left pulmonary arteries, one going to each lung. Within the lungs each artery branches extensively into smaller arteries and arterioles, then to capillaries. The pulmonary capillaries surround the alveoli of the lungs; it is here that exchanges of oxygen and carbon dioxide take place. The capillaries unite to form venules, which merge into veins, and finally into the two pulmonary veins from each lung that return blood to the left atrium. This oxygenated blood will then travel through the systemic circulation.

SYSTEMIC CIRCULATION

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The left ventricle pumps blood into the aorta, the largest artery of the body. We will return to the aorta and its branches in a moment, but first we will summarize the rest of systemic circulation. The branches of the aorta take blood into arterioles and capillary networks throughout the body. Capillaries merge to form venules and veins. The veins from the lower body take blood to the inferior vena cava; veins from the upper body take blood to the superior vena cava. These two caval veins return blood to the right atrium.

The aorta is a continuous vessel, but for the sake of precise description it is divided into sections that are named anatomically: ascending aorta, aortic arch, thoracic aorta, and abdominal aorta. The ascending aorta is the first inch that emerges from the top of the left ventricle. The arch of the aorta curves posteriorly over the heart and turns downward. The thoracic aorta continues down through the chest cavity and through the diaphragm. Below the level of the diaphragm, the abdominal aorta continues to the level of the 4th lumbar vertebra, where it divides into the two common iliac arteries. Along its course, the aorta has many branches through which blood travels to specific organs and parts of the body.

The ascending aorta has only two branches: the right and left coronary arteries, which supply blood to the myocardium.

The aortic arch has three branches that supply blood to the head and arms: the brachiocephalic artery, left common carotid artery, and left subclavian artery. The brachiocephalic (literally, “arm-head”) artery is very short and divides into the right common carotid artery and right subclavian artery. The right and left common carotid arteries extend into the neck, where each divides into an internal carotid artery and external carotid artery, which supply the head. The right and left subclavian arteries are in the shoulders behind the clavicles and continue into the arms. As the artery

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enters another body area (it may not “branch,” simply continue), its name changes: The subclavian artery becomes the axillary artery, which becomes the brachial artery. Some of the arteries in the head contribute to an important arterial anastomosis, the circle of Willis (or cerebral arterial circle), which is a “circle” of arteries around the pituitary gland. The circle of Willis is formed by the right and left internal carotid arteries and the basilar artery, which is the union of the right and left vertebral arteries (branches of the subclavian arteries). The brain is always active, even during sleep, and must have a constant flow of blood to supply oxygen and remove waste products. For this reason there are four vessels that bring blood to the circle of Willis. From this anastomosis, several paired arteries (the cerebral arteries) extend into the brain itself.

The thoracic aorta and its branches supply the chest wall and the organs within the thoracic cavity. The abdominal aorta gives rise to arteries that supply the abdominal wall and organs and to the common iliac arteries, which continue into the legs.

The systemic veins drain blood from organs or parts of the body and often parallel their corresponding arteries.

HEPATIC PORTAL CIRCULATION

Hepatic portal circulation is a subdivision of systemic circulation in which blood from the abdominal digestive organs and spleen circulates through the liver before returning to the heart.

Blood from the capillaries of the stomach, small intestine, colon, pancreas, and spleen flows into two large veins, the superior mesenteric vein and the splenic vein, which unite to form the portal vein. The portal vein takes blood into the liver, where it branches extensively and empties blood into the sinusoids, the capillaries of the liver. From the sinusoids, blood flows into hepatic veins, to the inferior vena cava and back to the right atrium. Notice that in this pathway there are two sets of capillaries, and keep in mind that it is in capillaries that exchanges take place. Let us use some specific examples to show the purpose and importance of portal circulation.

Glucose from carbohydrate digestion is absorbed into the capillaries of the small intestine; after a big meal this may greatly increase the blood glucose level. If this blood were to go directly back to the heart and then circulate through the kidneys, some of the glucose might be lost in urine. However, blood from the small intestine passes first through the liver

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sinusoids, and the liver cells remove the excess glucose and store it as glycogen. The blood that returns to the heart will then have a blood glucose level in the normal range.

Another example: Alcohol is absorbed into the capillaries of the stomach. If it were to circulate directly throughout the body, the alcohol would rapidly impair the functioning of the brain. Portal circulation, however, takes blood from the stomach to the liver, the organ that can detoxify the alcohol and prevent its detrimental effects on the brain. Of course, if alcohol consumption continues, the blood alcohol level rises faster than the liver’s capacity to detoxify, and the wellknown signs of alcohol intoxication appear.

As you can see, this portal circulation pathway enables the liver to modify the blood from the digestive organs and spleen. Some nutrients may be stored or changed, bilirubin from the spleen is excreted into bile, and potential poisons are detoxified before the blood returns to the heart and the rest of the body.

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PATHOPHYSIOLOGY

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Pathophysiology

Bite of Virus-Carrying MosquitoMosquito injects salivary secretion into skin’s blood vessel

Virus enters the bloodstream and initial replication occurs

Viremia occurs lasting until the fourth or fifth day after onset

Antibodies are produced principally against the virusAnd strong immune complex reaction occurs

Immune complex produce toxic substances like histamine, serotonin, bradykinin

Injured platelet Fever

Thrombocytopenia Headache

Proteinuria(+2)

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Pathophysiology

An infected Aedes Aegypti bites and injects salivary secretion (which contains an anticoagulant substance and dengue virus) into the skin’s blood vessel. The anticoagulant substance in the mosquitoe’s saliva helps suck blood well. As the virus enters the bloodstream, the initial replication occurred. The replication in the blood vessels results to viremia that lasts until the fourth or fifth day after onset.

Recent reports show that at first attack, neutralizing antibodies are produced principally against this virus type inoculated by the mosquito vector. The inflammants such as histamine, serotonin and bradykinin cause toxicity to the blood and blood vessels. There is thrombocytopenia due to diminished production and destruction of platelets. There is also fever and headache related to the immune response of the body against the invading microorganism. Thrombocytopenia may lead to signs and symptoms of bleeding such as proteinuria.

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Preventionand Treatment

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Prevention Vaccine development

There is no tested and approved vaccine for the dengue flavivirus. There are many ongoing vaccine development programs. Among them is the Pediatric Dengue Vaccine Initiative set up in 2003 with the aim of accelerating the development and introduction of dengue vaccine(s) that are affordable and accessible to poor children in endemic countries. Thai researchers are testing a dengue fever vaccine on 3,000–5,000 human volunteers after having successfully conducted tests on animals and a small group of human volunteers. A number of other vaccine candidates are entering phase I or II testing.

Mosquito control and other measures Use of mosquito repellent creams, liquids, coils, mats etc. Wearing of full sleeve shirts and full pants with socks Use of bednets for sleeping infants and young children during day time to

prevent mosquito bite As Aedes aegypti breeds in containers and receptacles detection & elimination of

mosquito breeding sources is the most important activity. Management of roof tops, porticos and sunshades Proper covering of stored water Reliable water supply Observation of weekly dry day Remove water from coolers and other small containers at least once in a week Use aerosol during day time to prevent the bites of mosquitoes Do not wear clothes that expose arms and legs Children should not be allowed to play in shorts and half sleeved clothes Use mosquito nets or mosquito repellents while sleeping during day time Avoid too many hanging clothes Destruction of breeding places Mesocyclops

In 1998, scientists from the Queensland Institute of Medical Research (QIMR) in Australia and Vietnam's Ministry of Health introduced a scheme that encouraged children to place a water bug, the crustacean Mesocyclops, in water tanks and discarded containers where the Aedes aegypti mosquito was known to thrive. This method is viewed as being more cost-effective and more environmentally friendly than

http://en.wikipedia.org/wiki/Mesocyclops

http://en.wikipedia.org/wiki/Vietnam

http://en.wikipedia.org/wiki/Australia

http://en.wikipedia.org/wiki/Queensland_Institute_of_Medical_Research

http://en.wikipedia.org/wiki/Clinical_trial#Phase_II

http://en.wikipedia.org/wiki/Clinical_trial#Phase_I

http://en.wikipedia.org/wiki/Thailand

http://en.wikipedia.org/wiki/Flavivirus

http://en.wikipedia.org/wiki/Vaccine

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pesticides, though not as effective, and requires the continuing participation of the community.

Even though this method of mosquito control was successful in rural provinces, not much is known about how effective it could be if applied to cities and urban areas. The Mesocyclops can survive and breed in large water containers but would not be able to do so in small containers that most urban dwellers have in their homes. Also, Mesocyclops are hosts for the guinea worm, a pathogen that causes a parasite infection, and so this method of mosquito control cannot be used in countries that are still susceptible to the guinea worm. The biggest dilemma with Mesocyclops is that its success depends on the participation of the community. This idea of a possible parasite-bearing creature in household water containers dissuades people from continuing the process of inoculation and, without the support and work of everyone living in the city, this method will not be successful.

WolbachiaIn 2009, scientists from the School of Integrative Biology at The University of

Queensland revealed that by infecting Aedes mosquitos with the bacterium Wolbachia, the adult lifespan was reduced by half. In the study, super-fine needles were used to inject 10,000 mosquito embryos with the bacterium. Once an insect was infected, the bacterium would spread via its eggs to the next generation. A pilot release of infected mosquitoes could begin in Vietnam within three years. If no problems are discovered, a full-scale biological attack against the insects could be launched within five years.

Mosquito mappingIn 2004, scientists from the Federal University of Minas Gerais, Brazil,

discovered a fast way to find and count mosquito population inside urban areas. The technology, named Intelligent Monitoring of Dengue (in Portuguese), uses traps with kairomones that capture Aedes gravid females, and upload insect counts with a combination of cell phone, GPS and internet technology. The result is a complete map of the mosquitoes in urban areas, updated in real time and accessible remotely, that can inform control methodologies. The technology was recognized with a Tech Museum Award in 2006.

Potential antiviral approachesDengue virus belongs to the family Flaviviridae, which includes the hepatitis C

virus, West Nile and Yellow fever viruses among others. Possible laboratory modification of the yellow fever vaccine YF-17D to target the dengue virus via chimeric replacement has been discussed extensively in scientific literature, but as of 2009 no full scale studies have been conducted.

In 2006 a group of Argentine scientists discovered the molecular replication mechanism of the virus, which could be specifically attacked by disrupting the viral RNA polymerase. In cell culture and murine experiments. morpholino antisense oligomers have shown specific activity against Dengue virus.

http://en.wikipedia.org/wiki/Oligomers

http://en.wikipedia.org/wiki/Morpholino

http://en.wikipedia.org/wiki/Mice

http://en.wikipedia.org/wiki/Cell_culture

http://en.wikipedia.org/wiki/Polymerase

http://en.wikipedia.org/wiki/Chimera_(virus)

http://en.wikipedia.org/wiki/Yellow_fever

http://en.wikipedia.org/wiki/West_Nile_virus

http://en.wikipedia.org/wiki/Hepatitis_C_virus

http://en.wikipedia.org/wiki/Hepatitis_C_virus

http://en.wikipedia.org/wiki/Flaviviridae

http://en.wikipedia.org/wiki/Dengue

http://en.wikipedia.org/wiki/Tech_Museum

http://en.wikipedia.org/wiki/Internet

http://en.wikipedia.org/wiki/GPS

http://en.wikipedia.org/wiki/Aedes

http://en.wikipedia.org/wiki/Kairomone

http://en.wikipedia.org/wiki/Federal_University_of_Minas_Gerais

http://en.wikipedia.org/wiki/The_University_of_Queensland

http://en.wikipedia.org/wiki/The_University_of_Queensland


http://en.wikipedia.org/wiki/Guinea_worm



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In 2007 virus replication was attenuated in the laboratory by interfering with activity of the dengue viral protease, and a project to identify drug leads with broad spectrum activity against the related dengue, hepatitis C, West Nile, and yellow fever viruses was launched

TreatmentBecause Dengue hemorrhagic fever is caused by a virus for which there is no known cure or vaccine, the only treatment is to treat the symptoms.

A transfusion of fresh blood or platelets can correct bleeding problems Intravenous (IV) fluids and electrolytes are also used to correct electrolyte

imbalances Oxygen therapy may be needed to treat abnormally low blood oxygen Rehydration with intravenous (IV) fluids is often necessary to treat dehydration Supportive care in an intensive care unit/environment Aspirin and non-steroidal anti-inflammatory drugs should be avoided as these

drugs may worsen the bleeding tendency associated with some of these infections. Patients may receive paracetamol preparations to deal with these symptoms if dengue is suspected

Oral fluid and electrolyte to prevent and correct dehydration Antipyretics/acetaminophen for fever Anticonvulsant like Dilantin for convulsions Sedatives may be needed to allay apprehension or agitation

Medical/Nursing Management Fluid Replacement

D5 0.3NaCl @ KVO rate upon admission D5 0.3NaCl x 8° (5/16/10) D5 LR 1L (5/17/10)

Laboratory Tests Hematology Urinalysis

Medications Paracetamol 500mg/tab q 4° for temp. 37.8°C Ascorbic Acid 500mg/tab OD Sucralfate 1gm/tab 1 tab q 8° PO prn Hyoscine N.Butylbromide 10mg/tab TID

http://en.wikipedia.org/wiki/Paracetamol

http://en.wikipedia.org/wiki/Non-steroidal_anti-inflammatory_drug

http://en.wikipedia.org/wiki/Aspirin





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Diet and Nutrition Diet as tolerated Avoid Dark Color Foods

Monitoring of Vital signs and signs of hemorrhage.

Health Teaching

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Patient and Family Health Teaching

Advise patient to comply medications as prescribed by the physician.

Advise the family to maintain a clean and safe environment.

Do tepid sponge bath if fever occurs. Encourage proper hygiene of the patient and family. Discuss possible source of infection Educate the family/pt on how to eliminate those vectors Never stock water in a container without cover Gallons, containers and tires must have proper way of

disposal Use insecticides at home Encourage family to clean the surroundings and clear

vegetations to destroy the breeding places of mosquitoes. Use of mosquito repellents and mosquito net.

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Nursing Care Plan


ASSESSMENT DIAGNOSIS PLANNING INTERVENTION EVALUATIONACTION RATIONALE

Subjective:“Wala namang masakit sakin” as verbalized.

Objective: Afebrile-

36.5°CPR-76RR-29BP-90/60

Platelet count-20x109/L

Thin extremities

Weakness (+2)

proteinuria Diet:DAT/

NDCF

Injury, risk for hemorrhage related to altered clotting factor

After nursing management, the client will be able to demonstrate behaviors that reduces the risk for bleeding

INDEPENDENT: Assess for

signs and symptoms of G.I. bleeding. Check for secretions. Observe color and consistency of stool

Observe for presence of petechiae, ecchymosis, bleeding from one or more sites.

Monitor pulse and blood pressure

.The G.I. tract is the most usual source of bleeding due to its mucosal fragility

Sub acute disseminated intravascular coagulation may develop secondary to altered clotting factors.

An increase

After nursing management, the client will be able to demonstrate behaviors that reduces the risk for bleeding and the patient will remain free from signs of hemorrhage


Note changes in mentation and level of consciousness

Encourage use of soft bristle toothbrush, avoiding straining for stool and forceful nose blowing.

Recommend avoidance of aspirin containing products.

COLLABORATIVE: Monitor Hgb,

Hct and Platelet count

in pulse with decreased bp may indicate loss of circulating blood volume.

Changes may indicate cerebral perfusion secondary to hypovolemia/hypoxemia

In the presence of clotting factor disturbances, minimal trauma can cause mucosal bleeding

Prolongs coagulation, potentiating


risk of

hemorrhage

Indicators of anemia, active bleeding or severity of coagulation defect.

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Drug Study


ASCORBIC ACIDVitamin C

Classification DosageMode Of Action

Indication Contraindication Adverse EffectsNursing

Responsibility

Vitamin/ Supplement

500mg/ tab OD

Water-soluble vitamin with antioxidantproperties; stimulates collagenformation and enhances tissue repair

➣Recommended dietary allowance➣Scurvy

contraindicated in diabetes mellitus,sodium-restricted diet, concurrentanticoagulant use, and history of recurrentrenal calculi,hypersensitivity totartrazine or sulfites (if product containsthese compounds), before testsfor occult blood in stool, and in breastfeedingpatients.

Transient mild soreness at I.M. or subcutaneousinjection site; transientlight-headedness or dizziness (withrapid I.V. administration)

>Avoid rapid I.V. infusion.>Don’t exceed recommendedamount in pregnant patients.


PARACETAMOLAcetaminophen



ResponsibilityAnalgesic, antipyretic

500mg/ tab q4° for temp. 37.8°C

Unclear. Pain relief may result from inhibitionof prostaglandin synthesis in CNS,with subsequent blockage of pain impulses.Fever reduction may result fromvasodilation and increased peripheralblood flow in hypothalamus, which dissipatesheat and

➣Mild to moderate pain caused byheadache,muscle ache, backache, minorarthritis, common cold, toothache,or menstrual cramps or fever

● Hypersensitivity to drug

Hematologic: thrombocytopenia, hemolyticanemia, neutropenia,leukopenia, pancytopeniaHepatic: jaundice, hepatotoxicityMetabolic: hypoglycemic comaSkin: rash, urticariaOther: hypersensitivity reactions (suchas fever)

Observe for acute toxicity and overdose.● Caution parents or other caregiversnot to give acetaminophen to childrenyounger than age 2 without consulting prescriber first.● Tell patient, parents, or other caregivers not to use drug concurrently with other acetaminophen-containing products.● Advise patient, parents, or othercaregivers to contact


lowers body temperature.

prescriber if fever or other symptoms persist despite taking recommended amount of drug.● Inform patients with chronic alcoholism that drug may increase risk of severe liver damage.● As appropriate, review all other significant and life-threatening adverse reactions and interactions, especially those related to the drugs, tests, and behaviors mentioned above.


SUCRALFATEApo-Sucralfate



Responsibility

GI protectant, Antiulcer agent

1gm/ tab 1tab q8° PO prn

Combines with gastric acid to formprotective coating on ulcer surface, inhibitinggastric acid secretion, pepsin,and bile salts

➣Active duodenal ulcer

none EENT: rhinitisGI: constipationRespiratory: respiratory difficultySkin: pruritus, rashOther: facial swelling, hypersensitivityreaction

● Monitor bowel pattern. Report severe,ongoing constipation.● Assess for rash and itching.● Tell patient to take 1 hour beforemeals and again at bedtime.● Caution patient not to take within 30minutes of antacids or other drugs.● Explain importance of completingentire course of therapy as prescribed,even after pain and other ulcer


symptomsimprove.● As appropriate, review all other significantadverse reactions and interactions,especially those related to thedrugs mentioned above

HYOSCINE Scopolamine Hydrobromide

Classification Dosage Mode Of Indication Contraindication Adverse Effects Nursing


Action Responsibility

Antimuscarinic, Antiemetic, Anticholinergic

10mg/ tab 1tab TID

Acts as competitive inhibitor at postganglionicmuscarinic receptor sitesof parasympathetic nervous systemand on smooth muscles that respondto acetylcholine but lack cholinergicinnervation. May block cholinergictransmission from vestibular nucleito higher CNS centers and fromreticular

➣Excessive GI motility and hypertoniain irritable bowel syndrome, milddysentery, diverticulitis, pylorospasm,and cardiospasm➣Preanesthetic sedation and obstetricAmnesia➣Postoperative nausea and vomiting➣Motion sickness

● Hypersensitivity to scopolamine,other belladonna alkaloids, or barbiturates● Hypersensitivity to bromides(injection only)● Angle-closure glaucoma● Acute hemorrhage● Myasthenia gravis● Obstructive uropathy (includingprostatic hypertrophy)● Obstructive GI disease (includingparalytic ileus and intestinal atony)● Reflux esophagitis● Ulcerative colitis or toxic megacolon● Hepatic or renal impairment● Chronic lung

CNS: drowsiness, dizziness, confusion,restlessness, fatigueCV: tachycardia, palpitations, hypotension,transient heart rate changesEENT: blurred vision,mydriasis, photophobia,conjunctivitisGI: constipation, dry mouthGU: urinary hesitancy or retentionSkin: decreased sweating, rash

.● Assess vital signs and neurologic,cardiovascular, and respiratorystatus.● Monitor patient for urinary hesitancyor retention.● Caution patient to avoid alcoholbecause it may increase CNSdepression.● As appropriate, review all other significantadverse reactions and interactions,especially those related to thedrugs, herbs, and behaviors mentioned


formation to vomitingcenter.

disease (with repeateddoses)

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EVALUATION

Upon admission, the patient was diagnosed with Dengue Fever, intermittent fever, diarrhea and vomiting were present. A D5 0.3NaCl was hooked at KVO rate. Decreased platelet (51x109/L) count and +2proteinuria were shown on the laboratory result. It is also shown in the results that there are decreased values of MCV and MCH which are indicative of anemia. WBC and neutrophils were decreased while monocytes were increased, which indicate severe viral infection. On the second day of confinement, diarrhea and vomiting were still present. The IV fluid infusion rate was changed to 40-41gtts/min and based on the laboratory result, the platelet count continued to decrease to 36x109/L. The patient is on DAT diet with restriction on dark-colored foods. On his third day on the hospital, the patient had no fever, diarrhea and vomiting but a great decreased on the platelet count (20x109/L) was noted. The patient should be observed and closely monitored for signs and symptoms of bleeding. Health teachings should be provided to the patient as well as to the family since they are the primary care giver, in order to prevent the development of further complication and to prevent any other family member from acquiring the same disease. And they should comply with the therapeutic regimen as ordered. They should be instructed to report any signs of bleeding to provide prompt intervention.

BIBLIOGRAPHY

Book References:Brunner and Suddarth,s Textbook of Medical and Surgical NursingTenth EditionSuzanne C. Smeltler, Brenda G. Bare

Essentials of Anatomy and Physiology8th EditionElaine Marieb

Eternal Links:www.nlm.nih.gov/medlineplus/ency/article/000223.htmen.wikipedia.org/wiki/Stomach_canceremedicine.medscape.com/article/375384-overviewwww.google.com

Others:Patient’s Chart

http://en.wikipedia.org/wiki/Stomach_cancer

casestudy dengue

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