ASSESSMENT A.

General Information Client’s initials: GEG Rm/Wd: Isolation Room (Medical Ward) Age: 28 Sex: Male OS: Single Nat. Filipino Race: Malay Educ. Attainment: undergraduate college Grade: A2C Length in service: 3 yrs Chief Complaint: fever Medical Diagnosis: SVI r/o DFS Admitting VS: T 37.9oC P 75 bpm BP: 100/70 mm Hg Weight 65 kg Allergies none Medications: none Beats/min R 25 cpm Ht. 5’8

Date Admitted: Aug. 24, 2009 Rel. Roman Catholic

B. Nursing History (Based on the Functional Health Pattern by Gordon) Date Performed: Aug. 26, 2009 1. HEALTH PERCEPTION-HEALTH MANAGEMENT PATTERN 1.1 Client’s description of her/his health Before Admission: “ Nilalagnat at masakit na ulo ko.” – as verbalized by the patient At present: “ Wala na akong masamang nararamdaman. Okay na ang pakiramdam ko. Gusto ko na nga bumalik sa trabaho.” – as verbalized by the patient 1.2 Health Management: Self- “ Nag-eexercise araw-araw. At kumakain pa lagi ng gulay.” – as verbalized by the patient Family and Children- “ Nasa Zamboanga ang pamilya ko kaya hindi ko sila nakakasama. Pero once na may magkasakit tumutulong naman ako. Nagpapadala ako ng perang pambili ng gamot.” – as verbalized by the patient 1.3 History of present illness: The present condition started 5 days prior to admission when the patient had undocumented fever and symptoms such as cough, colds, abdominal pain and vomiting. Patient self medicated with paracetamol 500mg/tab which afforded temporary lysis of the fever. Few hours prior to admission, patient consulted at the OPD where CBC c PC and urinalysis were done and revealed platelet of 198 x 10g/L, HCT of .48x10g/L and 10-15/hpf of RBC in the urinalysis. Patient was advised for admission. 1.4 Past illnesses: - unremarkable 1.5 History of hospitalization (when, where, and why) - He had been hospitalized 10 years ago at Zamboanga General Hospital because of minor operation in the left thumb. History of illness in the family: • (-) HPN • (+) OM- Paternal Side

1.6

2. NUTRITION AND METABOLIC PATTERN 2.1 Usual food (before admission) •Breakfast - rice, egg, fried foods, water •Lunch •Supper •Snacks - rice, soup, water, vegetables - rice, paksiw, water - none

•Type of Diet: no dark foods •Self feeding •Mouth condition: moist and pink Preferences: My client preferred to eat vegetable and dishes with soup. 2.2 Usual fluid intake (type, amounts): - My client drinks an estimated of more than 10 glasses per day. 2.3 2.4 Preferences: He preferred to drink coffee than soft drinks. Any food restrictions: - My client doesn’t have any food restrictions. Any problems with ability to eat: - My client eats well. He doesn’t any food problems.

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2.5

Any supplements (vitamins, feedings): none

3. ELIMINATION PATTERN 3.1 Bladder: Usual frequency/day: 4-5x/day Color: normally yellowish Complaints the usual pattern of urination: none 3.2 Bowel: Usual pattern/day (time, frequency, color and consistency) - My client usually remove bowel every other day. It is every morning. The bowel is normally brownish and semi-solid. Complaints of usual pattern of bowel movement: none 3.3 Skin: (condition) - My client’s skin tone is the same the general tone of her body. There’s a small scar on his left thumb. His skin is smooth, moist and warm. Skin is intact and no reddened areas. c IVF on R of PLRS 1L@350mL/0800Hx40gtts/min

4. ACTIVITY EXERCISE PATTERN 4.1 Usual daily/weekly activities - jogging everyday for 10 minutes, play basketball 4.2 Any limitations of physical ability: none 4.3 History of dyspnea or fatigue: none 5. SLEEP-REST PATTERN 5.1 Usual sleep pattern: Bedtime: 11 PM-7AM Hours slept: regularly 8 hrs. No. of pillows: 2 pillows Sleep routine: Before going to bed the patient take a shower and brush his teeth. Nap: none Feel rested and relaxed after sleep: yes 5.2 Any problems regarding sleep: none 5.3 Usual remedies: none 6. COGNITIVE-PERCEPTUAL PATTERN 6.1 Any deficits in sensory perception (hearing, sight, touch): - My client can clearly hear my voice. He can also see me and the things around him. He could also feel pain in her skin. Therefore, my client doesn’t have any deficits on hearing, seeing and touching. 6.2 Ability to read and write. Any difficulty in learning - My client can clearly read and properly write. He can understand my instructions and questions very well. He doesn’t have any problem in reading, writing and learning. 7. SELF-PERCEPTION PATTERN 7.1 What the client is most concerned about - My client is most concerned about to go out here in the hospital. He wants to go back to his work. 7.2 Present health goals - He wants to maintain a healthy and fit body and to avoid being sick again. 7.3 Appearance: calm, comfortable, appropriate dress and hygiene 7.4 Usual view of self?postive or negative? - “Parehas..depende sa sitwasyon pero madalas syempre positive.”-as verbalized by the patient 8. ROLE-RELATIONSHIP PATTERN 8.1 Language spoken: Filipino, English. Bisaya, Zamboanga’s language 8.2 Manner of Speaking: - My client speaks clear and her voice is modulated. I can clearly hear and understand the words that he is saying. 8.3 Significant person to client: - “Ang nanay ko ang pinaka close sa akin.” – as verbalized by the patient 8.4 Complaints regarding family: - “Wala naman kasi nga malayo sila sa akin at hindi ko sila nakakasama.” – as verbalized by the patient

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8.5 Living with (members of family) - “Nasa Zamboanga sila.Dito na ko sa barracks na ka stay.” – as verbalized by the patient 9. SEXUALITY-SEXUAL FUNCTION • • Is this person satisfied with his situation related to sexuality? – The patient is not sexually active. He doesn’t have any sexual partner. Does this person have any disease/ dysfunction of the reproductive system? – The patient doesn’t have any history of prostate problems, penile discharge and STD.

10. COPING-STRESS MANAGEMENT PATTERN 10.1 Decision making ability - “Depende sa sitwasyon. Kapag komplikado humuhingi ako ng advice sa nanay ko at mga kaibigan ko. Pero kadalasn ako na rin ang nagdedecide.” – as verbalized by the patient 10.2 Any significant stress in the past year - “Wala naman kasi hindi ko dinidibdib ang problema. Pag tapos na kinakalimutan ko na kaagad.” – as verbalized by the patient 10.3 Management of stress Lumalabas na lang ako kasama ng mga kaibigan.” – as verbalized by the patient 11. VALUE BELIEF SYSTEM 11.1 Source of strength or meaning: - “Ung nanay ko saka dasal sa diyos.” – as verbalized by the patient 11.2 Importance of God to client: - “Sa diyos ako nagdadasal kapag may problema pati pag may biyaya. Kasama siya sa buhay ko kahit anong nangyayari sa akin masaya man o malungkot.” – as verbalized by the patient 11.3 Religious practices (type and frequency): - The patient regularly attend mass every Sunday and always pray. 12. DEVELOPMENTAL TASKS (Assess for achievement of development tasks)

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The patient is at the stage of adulthood (age 28 years old) according to Erickson’s development stages, it has a central task of achieving generativity versus stagnation. He achieved his task for he had developed a positive resolution as evidenced by creativity, productivity, and her concern for others. He has a stable job, was able to help her parents and siblings financially and though he does not have a partner in life. He is not that self centered individual. With this task according to Erikson, our patient, had achieved a positive resolution. The patient has been single and has been living on her own away from her family. She had maintained an economic standard of living for herself and would sometimes help her family especially her siblings and mother. As a single man, the only way he could relate to other is through her work but not going into an intimate relationship. In their family it is also a common practice to be single. Based on Havighurst's Developmental Task Theory, the client has been able to cope up efficiently and effectively to the tasks necessary for her age though he was not able to have a partner in life.

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C. Physical Assessment Date Performed: August 26, 2009 V/S: BP= 120/80 mm Hg RR= 18 cpm General Appearance: - Conscious and coherent -

PR= 68 bpm Temp= 37.8oC

Smooth and steady gait; stands firm and erect No destructive mannerism or involuntary movements

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-

Speaks loud and modulated paced His physical appearance as well as his sexual development is apparent to his age and gender Weak in appearance Area assessed Technique Used Inspection Inspection Palpation Palpation Palpation Palpation Normal Findings Light to deep brown No lesions, scars or inflammation Smooth and even Moist Warm Skin pinches easily and immediately returns to its original position. Pink Convex No inflammation of the skin around the nail Hard and immobile Pink tone returns immediately to blanched nailbeds when pressure is released. Proportion to the body and the skull is rounded and smooth Symmetrical Black Straight and short No nits/lice present Evenly distributed No inflammation, lumps or masses Absence of seborrhea Light to deep brown Smooth Symmetric facial movement Evenly distributed, pupil is round, black and 2-3 mm in size, iris are brown, symmetrical and there no signs of lesions and markings Evenly distributed Equally aligned Evenly distributed, curved outward Pink Constrict when the light reflexed, pupils are equally round and reactive to light and acccomodation Same as facial color Actual Findings Light to deep brown No lesions, inflammation, have a scar on the left thumb Smooth and even Moist Hot Skin pinches easily and immediately returns to its original position. Pink Convex No inflammation of the skin around the nail Hard and immobile Pink tone returns immediately to blanched nailbeds when pressure is released. Proportion to the body and the skull is rounded and smooth Symmetrical Black Straight and short No nits/lice present Evenly distributed No inflammation, lumps or masses Absence of seborrhea Light to deep brown Smooth Symmetric facial movement Evenly distributed, pupil is round, black and 2-3 mm in size, iris are brown, symmetrical and there no signs of lesions and markings Evenly distributed Equally aligned Evenly distributed, curved outward Pink Constrict when the light reflexed, pupils are equally round and reactive to light and acccomodation Same as facial color Remarks Normal Scar is due to a minor operation Normal Normal Hyperthermia Normal

SKIN Color and pigmentation Lesions Texture Moisture Temperature Mobility and Turgor

NAILS Nail bed color Shape Lesions Texture Capillary refill

Inspection Inspection Inspection Palpation Palpation

Normal Normal Normal Normal Normal

HEAD Size Symmetry HAIR Color Texture Other Findings SCALP Distribution of hair Lesions Other Findings FACE Skin color Texture Facial movement EYES External structure

Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection

Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal

Eyebrows Eyelashes Eyelids Conjunctiva Pupillary reflexes

Inspection Inspection Inspection Inspection Inspection

Normal Normal Normal Normal Normal

EARS Color

Inspection

Normal

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Symmetry Shape and size Canal discharge NOSE Color Shape Discharges MOUTH Symmetry Color Moisture TONGUE Position Color Texture Mobility Lesions Gums Teeth Tonsils NECK Position Symmetry Range of movements

Inspection Inspection Inspection Inspection Inspection Inspection

Symmetrical at the level of the eyes corner Symmetric to head No discharges and inflammation Same as facial color Symmetric No discharges

Symmetrical at the level of the eyes corner Symmetric to head No discharges and inflammation Same as facial color Symmetric No discharges

Normal Normal Normal Normal Normal Normal

Inspection Inspection Palpation Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Inspection Palpation

Symmetric Pink Moist Positioned at the center, can move freely Dull red Smooth Can move freely No lesions or inflammation No lesion and no signs of bleeding No cavities No swelling, able to swallow Head centered Symmetrical Smooth movements without discomfort Symmetric and at midline position No swelling, enlargement, and tenderness Landmarks are positioned at midline. No masses or tenderness. Symmetrical chest expansion No tenderness No adventitious sound Equal size Symmetrical Evenly distributed Light to deep brown No lesions, deformities or inflammation No pain when moving, negative for masses and tenderness Equal strength bilaterally Flat and no dimplings, axillae doesn’t have a rash or infection noted Symmetric with ribs sloping downward at approximately 45oC degree angle in

Symmetric Pink Moist Positioned at the center, can move freely Dull red Smooth Can move freely No lesions or inflammation No lesion and no signs of bleeding No cavities No swelling, able to swallow Head centered Symmetrical Smooth movements without discomfort Symmetric and at midline position No swelling, enlargement, and tenderness Landmarks are positioned at midline. No masses or tenderness. Symmetrical chest expansion No tenderness No adventitious sound Equal size Symmetrical Evenly distributed Light to deep brown No lesions, deformities or inflammation No pain when moving, negative for masses and tenderness Equal strength bilaterally Flat and no dimplings, axillae doesn’t have a rash or infection noted Symmetric with ribs sloping downward at approximately 45oC degree angle in

Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal

Lymph nodes Thyroid gland

Palpation Inspection and Palpation

THORAX Chest Lungs UPPER EXTREMITIES Size Symmetry Distribution of hair Skin color Lesions Musculoskeletal functions

Inspection Palpation Auscultation Inspection Inspection Inspection Inspection Inspection Inspection

Normal Normal Normal Normal Normal Normal Normal Normal Normal

Brachial and radial arteries CHEST Breasts and axillae

Inspection Inspection

Normal Normal Normal

Thorax

Inspection

Normal

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Precordium Neck veins ABDOMINAL 4 Abdominal quadrants Liver Spleen Kidneys LOWER EXTREMITIES Size Symmetry Distribution of hair Skin color Lesions Musculoskeletal function

Palpation Auscultation Palpation Palpation Palpation Palpation Inspection Inspection Inspection Inspection Inspection Inspection

relation to the spine No pulsations or vibration No blowing or swishing Nontender and soft,no guarding and masses Not palpable Not palpable Not palpable Equal size Symmetrical Evenly distributed Light to deep brown No lesions, deformities or inflammation No pain when moving, negative for masses and tenderness strong and equal bilaterally

relation to the spine No pulsations or vibration No blowing or swishing Nontender and soft,no guarding and masses Not palpable Not palpable Not palpable Equal size Symmetrical Evenly distributed Light to deep brown No lesions, deformities or inflammation No pain when moving, negative for masses and tenderness Srong and equal bilaterally

Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal

Popliteal, posterior tibia and pedal arteries

Inspection

Normal

Summary of Abnormal Findings: SKIN Temperature- 37.8oC d/t hyperthermia Lesions- Scar on the left thumb d/t a minor operation Temperature- Cool d/t hypotension

REVIEW OF RECORDS CARDIOVASCULAR SYSTEM RESPIRATORY SYSTEM ENDOCRINE SYSTEM Because of the loss of blood or bleeding the patients heart compensate to this by increasing the cardiac output to supply all the needed in organs in the body and this cause tachycardia. Because of the increase cardiac output cause by bleeding the patient respiration also increase to supply enough oxygen to the body organs and cells. Because of bleeding there is low rate of erythrocyte that are circulating that contains oxygen. In this case a hormone called erythropoietin is being produced for the formation of erythrocyte and also there is decreased platelet and leukocytes, so there is increased colony stimulating factors thrombopoietin and interleukins released that is inside the bone (bone marrow) that helps in production of platelets.

LABORATORY EXAMINATIONS HEMATOLOGY REPORT Date: August 24, 2009 Time: 2:30PM PARAMETER Hematocrit NORMAL FINDINGS M: 0.40-0.54 ACTUAL FINDINGS 0.48 ANALYSIS Normal

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Platelet Count

150-450 x 10^g/L

163 x 10^g/dL

Normal

URINALYSIS REPORT Date: August 24, 2009 PARAMETER Color Transparency Reaction Specific Gravity Sugar Protein Squamous Epithelial Cells Red Blood Cells Pus Cells NORMAL FINDINGS Yellow Amber Clear to slightly turbid 4.5-8 1.005-1.030 Negative Negative Few Few Few ACTUAL FINDINGS Yellow clear 6.5 1.005 Negative Negative Occasional 0-2 0-2 ANALYSIS Normal Normal Normal Normal Normal Normal Normal Normal Normal

HEMATOLOGY REPORT Date: August 24, 2009 Time: 6:30PM PARAMETER Hemoglobin Hematocrit Platelet Count Lymphocytes NORMAL FINDINGS M: 130-180 g/dL M: 0.40-0.54 150-350 x 10^g/L 0.20-0.30 ACTUAL FINDINGS 136 g/dL .52 205 x 10^g/dL 0.42 ANALYSIS Normal Normal Normal Increased due to the body’s increased immune system

HEMATOLOGY REPORT Date: August 25, 2009 PARAMETER Hemoglobin Hematocrit Platelet Count NORMAL FINDINGS M: 130-180 g/dL M: 0.40-0.54 150-450 x 10^g/L ACTUAL FINDINGS 154 g/dL .51 250 x 10^g/dL ANALYSIS Normal Normal Normal

SEROLOGY REPORT Date: August 25, 2009 TEST Typhidot Typhidot NORMAL FINDINGS Negative Negative RESULT lgG lgM REMARK Negative Negative

Abnormal Findings; • Lymphocytes- 0.42 d/t the body’s increased immune system

INTRAVENOUS FLOW SHEET

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Date 8-24-09 3-11 11-7 8-25-09

Solution #1 D5LR1Lx30gtts/min #2 PLRx40gtts/min #3 PLRx40gtts/min

Time started 1600H 2200H 0600H

Amount to follow PLR1Lx40gtts/min #3PLRx40gtts/min #4 PLRx40gtts/min

3-11 11-7 8-26-09 7-3

#4 PLRx40gtts/min #5 PLRx40gtts/min #6 PLRx40gtts/min

1210H 2300H 1015H

#5 PLRx40gtts/min #6 PLRx40gtts/min #7 PLRx40gtts/min

Shift 8-24-09 3-11 8-25-09 7-3 3-11

I & O MONITORING Oral 500cc 500cc 600cc 450cc 480cc 1200cc

Urine

PATHOPHYSIOLOGY Exogenous pyrogens (virus carrier, infectious agents, toxins, tumors)

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Virus enters blood stream

Infects cells and generate cellular response (stimulates release of cytokines)

Cytokines destroys cell membrane and cell wall (viral antigens found in monocytes) Antipyretic Prostaglandin E2 Nonsteroidal anti-inflammatory drugs Anterior hypohtalamus

Elevated thermoregulatory set-point

(+) Heat conservation (vasoconstriction, behavior changes)

(+) Heat production (involuntary muscle contractions)

FEVER

When treated early with doctor prescribed medications and managed to prevent the appearance of other symptoms.

When illness become severe

Damage cell due to both cytokines and virus IVF’s and Electrolytes replacement and precautions Fluid shift from ICF-ECF Patient recovers

Manifest evanescent rashes

Rashes in several areas of the body

Bloody vomitus, urine, and stool

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Circulatory collapse

Shock

DEATH

DATA FROM THE TEXTBOOK Viral infections are common causes for upper and lower respiratory tract infections and a frequent reason for outpatient office visits. Comparatively, viral respiratory infections are less common in the intensive care unit (ICU) setting but still play an important clinical role. Most viral respiratory infections in the ICU are communityassociated cases with severe lower respiratory disease that can progress into respiratory failure and acute respiratory distress syndrome (ARDS). The remainder are infections seen in immunocompromised patients, such as transplantation]. In some instances (severe acute respiratory syndrome [SARS], influenza, and adenovirus), viral respiratory infections present with fulminant respiratory failure and ARDS, heralding a larger community outbreak. In these situations, the newly recognized illness in an ICU patient might be the first presentation of a larger public health emergency. The clinical presentation, treatment, outcome, and personal and institutional infection control differ greatly among the most common viral infections in the ICU. These differences are largely based on the viral structure, mode of transmission and cell entry, and host immunology and thus provide the foundation for the clinical presentation, virulence, and medical therapeutics of these viral infections. Therefore, a basic knowledge of the more common ICU viral respiratory pathogens will provide a framework for the clinical and research approaches for these infections. This review will focus on the basic epidemiology, virology, and host immune response for a few common or highimpact viral respiratory pathogens in the ICU: influenza, respiratory syncitial virus (RSV), SARS, varicella-zoster virus (VZV), adenovirus, cytomegalovirus (CMV), and viral hemorrhagic fever (VHF). With this basic foundation, clinical care, public health, and medical therapeutics for these viruses will be enhanced from the laboratory to the bedside. Influenza Influenza causes a clinically recognizable, systemic illness characterized by abrupt-onset fever, headache, myalgia, and malaise (the classic influenza-like illness). Influenza is subdivided into three distinct types: A, B, and C. Influenza A infects a variety of species, including birds, swine, horses, marine mammals, and humans. Influenza B infects only humans and predominates in children, and both influenza A and B cause yearly outbreaks. Respiratory symptoms are usually self-limited. However, a small number of individuals can develop primary pneumonia, which can progress to ARDS. The respiratory symptoms will persist or progress, and in a minority of cases ARDS can develop. The combination of pneumonia and ARDS usually occurs in at-risk individuals, like individuals with chronic lung diseases, but has been described in healthy individuals as well. The structure of influenza's viral envelope is important in viral infection and thus host cell immunity. The envelope contains surface glycoproteins essential for virus entry into the host cell. The trimeric hemagglutinin (HA) structure undergoes limited proteolysis by host cellular proteases such as furin. HA then binds to specific sialosaccharides found on the surface of respiratory epithelial cells to initiate cell entry. The neuraminidase (NA) is an enzyme that catalyzes the removal of terminal sialic acids from glycoproteins. This helps degrade respiratory tract mucus and release viral progeny after cell infection and thus is necessary for subsequent viral entry to viral escape from the host cell. Influenza A is divided into subtypes based on H and N antigenicity. All H subtypes have been found in multiple avian species and other animals. H1, H2, and H3 predominate in human disease seasonally, and more recently, avian subtypes such as H5 and H7 have increased in humans over the past decade. Infection occurs when viruses containing aerosols are deposited into the upper respiratory tract epithelium. In experimental volunteers, inoculation with small-particle aerosols more closely mimics natural disease than large drops into the nose, illustrating the easy transmission with coughing or sneezing. The virus can attach (HA) and penetrate the columnar epithelial cells. Predominantly human subtypes (H1, H2, and H3) bind to alpha-2,6-galactose sialic acid found in ciliated human respiratory tract epithelium. On the other hand, avian influenza subtypes (for example, H5N1) bind preferentially to alpha-2,3-galactose sialic acid, which is found in the gastrointestinal tract of water fowl, epithelial cells on human conjunctivae, and on human type 2 pneumocytes. This preferential binding for specific sialic acid receptors illustrates the differences in clinical presentation seen with avian influenza infections in humans: conjunctivitis, diarrhea, and fulminant alveolar pneumonia. Additionally, it underlies the difficulty with human-to-human transmission of avian strains as preferential binding to type 2 pneumocytes requires smaller particle aerosolization and deep inhalation into the alveoli rather than larger droplets seen with seasonal influenza transmission.

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Host immunity occurs via a number of mechanisms. Upon receptor binding, a large cytokine response occurs, with interleukin (IL)-2, IL-6, and interferon gamma predominately. This leads to extensive local inflammation with neutrophils and macrophages infiltrating the subepithelium of the respiratory tract. In cases of severe avian subtypes, a hemophagocytic syndrome and severe diffuse alveolar damage occur, causing the clinical findings of severe pneumonia and respiratory failure. Within the alveolar macrophages and pneumocytes, major histocompatibility complex (MHC) I up-regulation leads to antigen presentation of the HA and other subcapsular proteins. This eventually leads to natural killer cell destruction of infected cells and the development of neutralizing antibodies (largely against HA) by day 14 of infection. Treatment of active influenza involves antiviral agents and supportive care. The most effective therapy is prevention via vaccination and infection control. Two types of antiviral medications have been used: (a) M2 inhibitors (amantadine and rimantadine) inhibit the M2 ion channel needed for viral replication. These are not active against influenza B and C and resistance is common in seasonal influenza. Thus, they should be used only in cases of known susceptibility. (b) The NA inhibitors, oseltamivir and zanamivir, have less resistance and prevent cleavage of sialic acid, which is necessary for a new virus to exit from the host cell. Studies with the NA inhibitors show a reduction in symptom time and viral shedding, with peak effect when started within 48 hours of symptom onset However, treatment with NA inhibitors after 48 hours may provide some additional benefit but has not been fully studied. Resistance is low within the community, but NA inhibitor resistance has already been described in clinical isolates from human cases of avian influenza. Respiratory syncytial virus Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract infections in children under 1 year of age, and healthy adults are infected repeatedly throughout their lives. Adults typically have upper respiratory tract symptoms; however, some adults will develop lower respiratory tract infections, including bronchiolitis, pneumonia, and (rarely) ARDS. The elderly and immunocompromised, particularly bone marrow transplant patients, are at highest risk of lower respiratory tract infection and respiratory failure. In these cases, upper airway infection usually precedes lower tract infection by 1 to 3 days. Infection follows a pattern similar to influenza, with epidemics occurring in the winter months. Inoculation occurs at the nasal or ocular mucosa via direct contact with secretions or infected fomites. RSV has a lipoprotein envelope with surface glycoproteins that are important in host infection. These glycoproteins act as cell fusion proteins, ultimately forming multinucleated giant cells ('syncytia'), assisting in cell-to-cell spread. The virus replicates locally and then spreads to the epithelium of the bronchioles. From the bronchioles, the virus can then extend to the type 1 and 2 alveolar pneumocytes. Infection leads to cellular (neutrophils, monocytes, and T cells) infiltration of the epithelium and supplying vasculature, with subsequent necrosis and proliferation. This will cause the airway obstruction, air trapping, and increased airway resistance that are characteristic of RSV infection. RSV infection is more specifically associated with IL-6 and macrophage inflammatory protein-1 (MIP-1) release. Elevated levels of IL-6 and MIP-1 in the bronchioles have correlated with more severe disease. Both droplet and contact transmissions are the main methods of spread, and thus hand washing, droplet isolation, and the use of personal protective equipment are all important in reducing viral spread. Specific genotypes will predominate during a seasonal outbreak, and since the genotypes change annually, adult reinfections occur. Treatment usually is focused on controlling bronchospasm and preventing spread to other patients and health care workers. Bronchodilators and corticosteroids are used for bronchospasm, and aerosolized ribivirin has been used in severe and high-risk cases such as bone marrow transplants. However, a recent study evaluating bronchiolitis in infants, in which over 50% of cases were caused by RSV, showed that corticosteroids had no effect on outcome. Severe acute respiratory distress syndrome SARS is caused by a novel coronavirus (SARS-CoV) that was first detected in 2003. The initial outbreak rapidly spread into a global epidemic, with cases reported from 29 countries. The fatality rate was 11%, with most deaths in patients older than 65 and no deaths in children. Since the initial epidemic in 2003, no new cases have been reported. SARS appears to clinically present as a two-stage illness. The initial prodrome, characterized by fever with or without rigors, malaise, headache, and myalgias, occurs an average of 7 days after contact with infected individuals. Some patients also have mild respiratory symptoms or nausea and diarrhea. The respiratory phase appears to develop approximately 8 days after the onset of fever. Forty-five percent of patients will develop hypoxemia and approximately 20% of these patients will progress to acute lung injury and require mechanical ventilation. SARSCoV appears to have originated from the horseshoe bat. The horseshoe bat appeared to be a natural reservoir for the virus and the civet cat acted as an intermediate host, allowing transmission to humans. Like RSV and influenza, SARS-CoV has a lipoprotein envelope, but unlike the RSV and influenza, the virus is assembled and obtains its envelope from the endoplasmic reticulum. SARS-CoV, like other coronaviruses, starts with infection of the upper respiratory tract mucosa. SARS-CoV binds to CD209L (L-SIGN) and ACE-2, two functional receptors on the respiratory tract epithelium. After binding, local inflammation and edema increase. ACE-2 has a key protective role in acute lung injury by reducing alveolar fluid, and thus the binding of SARS-CoV to ACE-2 may contribute to the dysregulation of fluid balance in the alveolar space. Additionally, low mannosebinding lectin (MBL) levels are thought to play a role in SARS pathogenesis. In many respiratory infections, MBL prevents receptor attachment, activates complement, and enhances phagocytosis. In SARS-CoV infections, low or deficient levels of MBL have been noted, particularly associated with an MBL haplotype. The binding of SARSCoV to ACE-2, along with lower levels of MBL, leads to higher viral levels, increased alveolar edema, and the severe acute respiratory failure associated with SARS-CoV. Viral spread is by droplet transmission, although many cases suggest that airborne and contact routes also occur. Spread to health care workers who wore appropriate personal protective equipment suggests an airborne mode, and additional spread by aerosol-generating procedures, such as resuscitation (cardiopulmonary resuscitation), medication nebulization, and noninvasive ventilation, further supports this mode. The treatment for SARS is largely supportive with low tidal volume mechanical ventilation. Numerous treatment strategies, including corticosteroids, ribavirin, immunoglobulin, and interferon, have been investigated in SARS: none has been demonstrated to provide clinical evidence of benefit.

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Varicella-zoster virus VZV infection routinely occurs during childhood, presenting with low-grade fever, malaise, pharyngitis, and a vesicular rash. Primary disease occurs throughout the year and usually is self-limited in immunocompetent host. VZV pneumonia is rare in children. However, it is the most frequent complication in adults (20%) and accounts for the majority of hospitalizations from VZV. Varicella pneumonia develops insidiously, usually a few days after the onset of rash, and can progress to respiratory failure and ARDS. Risk factors for VZV pneumonia and ARDS include pregnancy, smoking, and immunosuppression (malignancy, corticosteroids, HIV, and solid-organ transplant), but young healthy adults rarely develop ARDS. Mortality for VZV pneumonia is 10% to 30%, with a mortality of 50% when respiratory failure ensues. Additional complications include encephalitis, hepatitis, and secondary skin and soft tissue infections. VZV is a herpes virus, a common group of DNA viruses that have a lipid-containing envelope with surface glycoproteins. Infection starts in the upper respiratory tract mucosa as the surface glycoprotiens allow for fusion of the lipid envelope with the respiratory cell membrane. Upon cell entry, viral replication and assembly occur after integration of the viral genes into the cellular DNA. Naked capsids then acquire their envelope at the nuclear membrane and are released into the perinuclear space where large vacuoles are formed, leading to the clinical vesicles. Local replication and spread lead to seeding of the reticuloendothelial system and ultimately viremia, which leads to diffuse and scattered skin lesions associated with primary varicella. Viral shedding can last from onset of fever until all lesions have crusted and pneumonia has improved. Both humoral immunity and cell-mediated immunity are involved in protection. Antibodies are directed at the surface glycoprotein and lead to viral neutralization. Cellular immunity drives local inflammation, leading to cell repair and vacuole removal. The virus becomes latent within the dorsal root ganglia. During latency, the viral DNA is located in the cytoplasm rather than integrated into nuclear DNA. VZV is highly contagious and transmission is via respiratory droplets and direct contact with lesions. The envelope is sensitive to detergent and air drying, which account for the lability of VZV on fomites. In adults who progress to pneumonia or ARDS, treatment with acyclovir and corticosteroids has been shown to lessen hospital and ICU stays. In immunocompromised persons not previously exposed to VZV, varicella-zoster immune globulin has been shown to be useful for both prevention of disease and symptomatic improvement. Adenovirus Adenovirus is the one of the most common causes of upper respiratory tract infections in adults and children. Clinical disease usually is a self-limited upper respiratory tract infection associated with conjunctivitis; however, severe lower respiratory disease can occur in both high-risk and healthy individuals. The combination of pneumonia and ARDS develops in a minority of individuals and usually is associated with conjunctivitis and other extrapulmonary manifestations, such as gastrointestinal disease, hepatitis, meningitis, and hemorrhagic cystitis. The extrapulmonary complications, along with ARDS, are more frequent in transplant recipients. Pneumonia and ARDS appear to be more common with subtype E type 4 and subgroups B type 7, but serogroup 35 also has been documented in mental health facilities. Recent increases in respiratory diseases in adults have been noted over the past year with serotype 14. Over 51 human adenovirus subtypes exist and clinical syndromes vary among subtypes. However, certain subtypes appear to have an increased likelihood of lower respiratory tract involvement and this appears to be related to the viral capsid proteins. Unlike influenza, RSV, and SARS, adenovirus is a DNA virus covered by a protein capsid without a lipid envelope. Rodlike structures called fibers are one of three capsid protein types (hexons, pentons, and fibers) and these fibers are the attachment apparatus for viral adsorption to the cell. Attachment occurs at the coxsackieadenovirus receptor, the same receptor as the coxsackie B virus. The hexon capsid protein appears to have some antigenic sites that are common to all human adenoviruses and contains other sites that show type specificity. Fiber antigen seems to be primarily type-specific with some group specificity, whereas the penton base antigen is common to the adenovirus family. Upon infection, respiratory epithelial cells express these capsid proteins on their surface, leading to direct CD8+cytotoxic T-cell MHC class 1 killing of these cells. Thus, epithelial destruction associated with submucosal edema drives the clinical findings of lower respiratory disease. Additionally, neutralizing antibody is directed at the hexon type-specific antigen and provides some future protection against serotypes. Adenovirus is relatively stable on environmental surfaces for long periods of time, and thus viral spread is largely associated with infected fomites. Spread also occurs via droplet transmission. Treatment is largely supportive. For severe cases, especially in immunosuppressed patients, antiviral therapy has been attempted but no clinical studies exist. In severe cases, especially in immunocompromised patients, ribavirin and cidofovir antiviral therapy has been attempted, but no controlled clinical trials exist. Cytomegalovirus CMV is a common viral infection that causes both primary and latent infections. Seroprevalence rates range from 60% to 70% in US adult populations. CMV causes a wide spectrum of illness, ranging from an asymptomatic infection to a mononucleosis syndrome, organ-specific complications, and fulminant multisystem disease. Immunocompetent patients are more likely to present with minimal to no symptoms, whereas immunocompromised patients are more likely to develop organ-specific complications and fulminant disease. The most significant and severe disease syndromes are found in lung, liver, kidney, and heart transplant recipients. Significant morbidity and mortality usually are confined to immunocompromised persons; however, previously healthy individuals can present with organ-specific complications or even present with fulminant disease. CMV is a member of the herpes virus family and, like other members of this family, is known for causing latent infections. Like other herpes viruses, CMV is an enveloped virus with multiple surface glycoproteins. These glycoproteins are important for viral entry into host cells and are targets for host cell humoral and cell-mediated immunity. The cellular protein that serves as the specific receptor for CMV entry has not been identified, but CMV infects cells by a process of endocytosis. Once entry has occurred, CMV alters host immunity through the activation

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of multiple genes. One important CMV protein prevents cellular HLA-1 molecules from reaching the cell surface, preventing recognition and destruction by CD8+ T lymphocytes. Thus, the CMV genome can remain in infected cells and avoid immune destruction, which accounts for its latency in clinical disease. Eventually, a cellular immune response, driven by high levels of anti-CMV CD4+ and CD8+ T cells, leads to control of the disease. Antibodies against CMV do not provide significant immunity. Avoiding immune detection gives CMV the ability to remain latent after infection, which contributes a great deal to serious CMV disease. Evidence for persistent CMV genomes and antigens exists in many tissues after initial infection, and CMV has been found in circulating mononuclear cells and in polymorphonuclear neutrophils. The virus can be cultured from most bodily fluids, including blood, urine, stool, tears, semen, and breast milk, and from mucosal surfaces, including the throat and cervix. Detection of cells that contain CMV intranuclear inclusions in renal epithelial tissue and in pulmonary secretions provides evidence that CMV may persist in these tissues as well. CMV antigens have also been detected in vascular endothelial cells; this site has been suggested as a cause of vascular inflammation and development of atherosclerosis. When immune suppression occurs in patients by means of HIV infection or through immunosuppressive therapy, such as antilymphocyte antibody infusion, CMV can reactivate, producing end-organ disease. Specifically from a pulmonary standpoint, CMV is common after lung transplantation, causing an acute pneumonitis or contributing to a chronic bronchiolitis. In HIV patients, CMV pneumonitis is rare but postmortem studies suggest that pulmonary disease from CMV occurs at higher rates than previously recognized. CMV is transmitted via many routes. Transmission has been observed among family members (thought to be secondary to close contact and viral shed from the upper respiratory tract), among children and employees at daycare centers, from sexual contact, blood and tissue exposure (seroconversion after transfusion of blood products or organ transplantation), and perinatally (during birth or from breast milk). There are several antiviral agents available for systemic treatment of CMV. These agents include ganciclovir, valgancicilovir, foscarnet, and cidofovir. Viral hemorrhagic fevers The VHFs include a wide number of geographically distributed viruses found worldwide, including Ebola and Marburg viruses, Rift Valley fever, Crimean Congo hemorrhagic fever, Lassa fever, yellow fever, and dengue fever. Ebola and Marburg viruses are in the family filoviridae. Although the underlying pathophysiology differs slightly between the VHFs, Marburg and Ebola viruses serve as a classic template. Marburg virus has a single species whereas Ebola has four different species that vary in virulence in humans. The clinical manifestations of both Marburg and Ebola viruses are similar in presentation, with a higher mortality with Ebola Zaire (75% to 90%) than Marburg (25% to 40%) virus being the only major difference between them. The initial incubation period after exposure to the virus is 5 to 7 days, with clinical disease beginning with the onset of fever, chills, malaise, severe headache, nausea, vomiting, diarrhea, and abdominal pain. With this initial infection, macrophages and dendritic cells initially are the site of viral replication, followed by spread to the reticuloendothelial system heralding the initial onset of symptoms. As macrophages and other infected tissues undergo necrosis, an overwhelming cytokine response occurs, leading to abrupt prostration, stupor, and hypotension. Particularly, tumor necrosis factor (TNF), IL-1, IL-6, macrophage chemotactic protein, and nitric oxide levels are markedly increased. VHF-infected macrophages, along with noninfected macrophages stimulated by cytokines, release cell surface tissue factor, which subsequently triggers the extrinsic coagulation pathway. The clinical and laboratory findings of impaired coagulation with increased conjunctival and soft tissue bleeding shortly follow. In some cases, more massive hemorrhage can occur in the gastrointestinal and urinary tracts, and in rare instances, alveolar hemorrhage can occur. The onset of maculopapular rash on the arms and trunk also appears to be classic and may be a very distinctive sign. Along with the bleeding and hypotension, multiorgan failure occurs, eventually leading to death. The overwhelming viremia resulting in macrophage and dendritic cell apoptosis leads to impaired humoral immunity, which in turn leads to increase viral production. This ultimately results in the rapid overwhelming shock seen with VHFs. Transmission appears to occur through contact with nonhuman primates and infected individuals. No specific therapy is available and patient management includes supportive care. In a few cases in the Zaire outbreak of Ebola in 1995, whole blood with IgG antibodies against Ebola may have improved outcome, although subsequent analysis suggests that these patients were likely to survive even without this treatment. Hantavirus Hantavirus is one of four major genera within the family bunyaviridae, a family of more than 200 animal viruses spread via arthropod-vertebrate cycles. Hantavirus causes two severe acute febrile illnesses: hemorrhagic fever with renal syndrome (HFRS) (found in the Old World) and Hantavirus cardiopulmonary syndrome (HPS) (found in the New World). HPS was first classified in the Southwestern US. A new species termed Sin Nombre virus was identified after an outbreak in the Four Corners region of the Southwestern US in 1993. In North America, disease largely has been reported in the Southwest and California, with cases reported in Canada, Europe, China, Chile, Argentina, and other parts of South America. Outbreaks are often cyclical and focal and are affected by weather and climatic variables and the effect this has on rodent populations. Symptoms begin with a prodrome of fever, chills, and myalgias; HFRS and HPS also can be accompanied by abdominal pain and gastrointestinal disturbances. In HPS, initially, there is an absence of upper respiratory symptoms. At about day 5, modest dry cough and dyspnea will develop. Due to the severe increase in vascular permeability associated with HPS, disease progresses rapidly (within hours) to respiratory failure, shock, ARDS, coagulopathy, and arrhythmias. Resolution also can occur rapidly. If hypoxia is managed and shock is not fatal, the vascular leak reverses in a few days and recovery is apparently complete. Notably, thrombocytopenia with an immunoblast-predominant leukocytosis is characteristic of the early cardiopulmonary phase The exact mechanism for ARDS, shock, and coagulopathy is unclear, but it is suspected that the immune response, rather than the virus itself, causes the capillary leak and shock. The intense cellular immune response alters endothelial cell barrier function and is harmful. Hantavirus causes an increased release of TNF and alpha interferon and increased MHC I antigen presentation. There is also a more intense CD8+ T-cell response in sicker patients. It

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appears to result from a massive acute capillary leak syndrome and shock-inducing mechanisms thought to be due to the release of kinins and cytokines. The syndrome's clinical presentation, rapid resolution, and histopathologic findings of interstitial infiltrates of T lymphocytes and alveolar pulmonary edema without marked necrosis support this underlying process. Treatment mainly is supportive, with extracorporeal membrane oxygenation being used in some cases. Ribavirin has been effective in HFRS, but not HPS. Mortality remains at roughly 20%. Conclusion Viral infections in the ICU are common in the outpatient setting but become less common in the ICU. However, a small number of viral infections can lower respiratory tract disease and subsequent respiratory failure. These viral pathogens vary greatly in clinical disease, from rapid and fulminant respiratory failure and shock (VHF) to chronic latent disease of immunosuppression (CMV). However, most of these viruses commonly have lipid envelopes, except for adenovirus, and all have surface proteins or glycoprotiens that allow for attachment, cell entry, and virulence. Host response to these infections varies from primarily cellular to humoral. All can cause respiratory disease but a few are of great public health concern, particularly novel strains of influenza, adenovirus, SARS, and VHFs. An understanding of the basic viral pathogenesis, along with host response, allows for a foundation in treatment and public health response within the ICU. Bacterial or viral Bacterial and viral infections can both cause symptoms such as malaise, fever, and chills. It can be difficult, even for a doctor, to distinguish which is the cause of a specific infection. It's important to distinguish, because viral infections cannot be cured by antibiotics.

Comparison of viral and bacterial infection

Characteristic

Viral

Bacterial

Typical symptoms

The classic symptoms of a bacterial infection are localized redness, heat, swelling and pain. One of In general, viral infections are systemic. This the hallmarks of a bacterial infection is local pain, means they involve many different parts of the pain that is in a specific part of the body. For body or more than one body system at the same example, if a cut occurs and it is infected with time; i.e. a runny nose, sinus congestion, cough, bacteria, pain will occur at the site of the body aches etc. They can be local at times as in infection. Bacterial throat pain is often viral conjunctivitis or "pink eye" and herpes. Only characterised by more pain on one side of the a few viral infections are painful, like herpes. The throat. An ear infection is more likely to be pain of viral infections is often described as itchy bacterial if the pain occurs in only one ear. An or burning. infection that produces pus is not always bacterial.

Cause

Pathogenic viruses

Pathogenic bacteria

What Causes Viral Infections? Human cells are vulnerable to viruses, and when the body is exposed to viral particles, the immune system will try to destroy these particles and eliminate them from the system. A lowered immune system allows the virus to more easily attach itself to available cells, often bringing about general symptoms such as fever, chills, and muscle aches. This also makes it easier for the virus to replicate, and thus advances symptoms until the immune system can fight the virus off. Help for Viral Infections The best way of treating human viruses will depend on the strength of the individual’s immune system, their overall health status, age, the severity of the condition, and the type of viruses involved. View products related to Viral Infection Minor illnesses caused by viral infections usually only require symptomatic treatment, while more severe conditions may require advanced medical treatment and sometimes even life-long treatment. A combination of treatment options such as conventional medicine, complementary therapy, and natural medicine can help to fight the infection, control the symptoms, and strengthen the immune response.

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It is important to remember that treating human viruses cannot be accomplished through antibiotics, and the unnecessary use of antibiotics can weaken the immune system, thus increasing the likelihood of contracting another infection. Conventional Medicine for Viral Infections • • Over-the-counter painkillers and anti-inflammatories such as paracetamol or ibuprofen can reduce symptoms and fever, but can also have side effects, especially with long-term or excessive usage. Antiviral medication and immune substances such as interferons and immunoglobulins are sometimes prescribed for more serious infections. They can be administered orally, intravenously, intramuscularly, topically, or by inhalation. Because viruses live within the body’s own cells, antiviral medications often have severe side effects. In order to kill off the virus, they have to damage the body’s cells. Antiretroviral therapy suppresses the replication of the human immunodeficiency virus (HIV), even if there are no symptoms. The aim of treatment is to lower the concentration of virus (viral load).

Natural Herbal and Homeopathic Remedies for Viral Infection Natural and holistic remedies used instead of or in conjunction with conventional medicine and other complementary therapies can be extremely effective in relieving the symptoms of viral infections and treating human viruses. These types of remedies can successfully address the underlying cause of the condition as well as help to maintain the overall physical and emotional health of the individual. Herbal and homeopathic remedies are gentle and safe to use without the harmful side effects of many prescription medications. Hypoxis rooperi, Agothosma betulina, Mentha piperita, Solidago virgaurea, Viscum album, Crataegus oxycanthoide, Schizandra sinesis, Astralagus membranaceus, and Olea europea are all examples of natural remedies that can help to promote immune system functioning and support the body’s ability to fight against harmful pathogens. Consult a physician, homeopath, or herbalist about a remedy that suits you.

Complementary Therapy • • • • • Acupuncture Herbal and homeopathic remedies Aruyvedic medications Nutritional therapy Meditation, psychotherapy, and counseling may be of benefit when there are long-term consequences and psychological implications.

Physical examination » Tests and diagnostic procedures » Clinical laboratory tests » Body fluid tests » Blood Blood is composed of plasma and blood cells. The blood cells—erythrocytes (red blood cells), leukocytes (white blood cells), and thrombocytes (platelets)—are suspended in the plasma with other particulate matter. Plasma is a clear, straw-coloured fluid that makes up more than half the volume of blood. It is distinguished from serum, the clear, cell-free fluid in which fibrinogen has been converted to fibrin and from which some clotting proteins have been removed. Serum is formed when the plasma or whole blood is allowed to clot. Centrifugation can be used to separate the plasma or serum from blood samples. Tests to measure the concentration of substances in the blood may use plasma, serum, or whole blood that has been anticoagulated to keep all the contents in suspension. A complete blood count (CBC) is a measure of the hematologic parameters of the blood (see the table for reference values). Included in the CBC is the calculation of the number of red blood cells (red blood cell count) or white blood cells (white blood cell count) in a cubic millimetre (mm3) of blood, a differential white blood cell count, a hemoglobin assay, a hematocrit, calculations of red cell volume, and a platelet count.

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The differential white blood cell count includes measurements of the different types of white blood cells that constitute the total white blood cell count: the band neutrophils, segmented neutrophils, lymphocytes, monocytes, eosinophils, and basophils. A specific infection can be suspected based on the type of leukocyte that has an abnormal value. Viral infections usually affect the lymphocyte count, whereas bacterial infections increase the percentage of band neutrophils. Eosinophils are increased in those with allergic conditions and some parasitic infections. Infection with human immunodeficiency virus (HIV), which causes acquired immunodeficiency syndrome (AIDS), damages the body’s ability to fight infection. The immune system of a healthy individual responds to infection by increasing the number of white blood cells; however, the immune system infected with HIV is unable to mount a defense of white blood cells (namely, lymphocytes) and cannot defend the body against viral, bacterial, or parasitic assault. Calculations of red blood cells provide important information on the possible etiology (origin) of a disease. For example, the mean corpuscular volume (MCV) is the most useful indicator for anemia. The reticulocyte count, which measures the number of young red blood cells being produced, is used to distinguish between anemias resulting from a decrease in production of erythrocytes and those caused by an increase in destruction or loss of erythrocytes. An increase in the number of red blood cells (polycythemia) is normal for persons living at high altitudes, but in most of the population it indicates disease. Platelets, small structures that are two to four micrometres in diameter, play a role in blood clotting. A decrease in the platelet count can result in bleeding if the number falls to a value below 20,000 platelets per microlitre. Counts above 50,000 to 100,000 per microlitre may be required for invasive or surgical procedures. In addition, platelet function is also important. For example, patients with a normal platelet count who have been on antiplatelet drugs such as aspirin may have increased or severe bleeding when subjected to cardiovascular surgical procedures. Hematopoiesis (the production of blood cells) occurs in the bone marrow, and many types of blood disorders can be diagnosed best by analyzing a sample of bone marrow removed by a needle from the centre of the pelvic bone or the sternum (bone marrow biopsy). Bleeding disorders are suspected when blood is seen in the skin (purpura) or a wound is delayed in clotting. In addition to a low platelet count in the peripheral blood, there may be a decrease in megakaryocytes, cells in the bone marrow that form platelets. A bleeding time greater than 20 minutes indicates an abnormality of platelet function. Other screening tests for coagulation disorders include the prothrombin time (PT) test, the activated partial thromboplastin time (APTT) test, and the plasma fibrinogen assay. Specific procoagulant proteins, which are enzymes essential to the clotting of blood, should be assayed if a disorder associated with one of them is suspected. For example, factor VIII or IX can be assayed if the patient is thought to have hemophilia A or B, respectively. Deep-seated hemorrhages into joints or tissue spaces after apparent minor trauma and a family history of bleeding disorders may indicate hereditary hemophilia. The erythrocyte sedimentation rate (ESR) is the rate at which red blood cells settle in a column of blood in one hour. It is a nonspecific indicator of inflammatory disease that is also increased in anemia.

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The Coombs, or antiglobulin, test (AGT) is used to test red blood cells for compatibility when doing a cross match between donor red blood cells and recipient serum. The AGT test detects antibodies that would cause lifethreatening immune destruction during the transfusion of red blood cells. It also is used to detect antibodies to red blood cells in hemolytic disease of the newborn and drug-induced hemolytic anemias.

Physical examination » Tests and diagnostic procedures » Clinical laboratory tests » Body fluid tests » Urine Examining the urine is one of the oldest forms of diagnostic testing, extending back to the days of Hippocrates. Physicians observed the urine (uroscopy) to diagnose all forms of illness because direct examination of a patient, or at least disrobing the patient, was socially unacceptable (see above Historical aspects). Urinalysis is the most commonly performed test in the physician’s office. It consists of (1) a gross examination, in which the colour, turbidity, and specific gravity of the urine are assessed, (2) the use of a dipstick (a plastic strip containing reagent pads) to test for bilirubin, blood, glucose, ketones, leukocyte esterase, nitrite, pH, protein, and urobilinogen, and (3) a microscopic examination of a centrifuged specimen to detect red or white blood cells, casts, crystals, and bacteria. The urine is collected using a “clean-catch” technique to eliminate contamination with bacteria from skin or vaginal secretions. Dipstick tests are available that contain from 2 to 10 different tests. The test for glucose, which likely indicates diabetes, and the test for protein, which indicates kidney disease, tumours of the urinary tract, or hypertensive disorders of pregnancy, are two of the most important assays available. The microscopic examination is the most valuable urinalysis test. It will show a variety of cells that are normally shed from the urinary tract. Usually up to five white blood cells per high-power field (HPF) are present; more than 10 white blood cells per HPF indicates a urinary tract infection. Red blood cells in the urine sediment can be indicative of urinary tract inflammation and can also be a sign of a malignant tumour of the kidney, bladder, or urinary tract. More than two red blood cells per HPF is abnormal, although in women this is often due to vaginal contamination from menstruation. The identification of red blood cells in the urine (hematuria) always demands follow-up to determine the cause and to rule out the presence of a neoplasm (tumour). Cylindrically shaped urinary casts, shed from the kidney’s tubules, consist of protein mixed with cells or other materials and may indicate renal disease if present in large numbers. Various crystals also are found in the urinary sediment, but these are generally of little clinical significance. Occasionally, the presence of specific crystals may help confirm a diagnosis; for example, uric acid crystals in the urine may be associated with gout.

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REVIEW OF ANATOMY AND PHYSIOLOGY CARDIOVASCULAR SYSTEM

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The Circulatory System is the most important system of your body. It is responsible for transporting materials throughout the entire body. It transports nutrients, water, and oxygen to your billions of body cells and carries away wastes such as carbon dioxide that body cells produce. It is an amazing highway that travels through your entire body connecting all your body cells. Blood moving away from the heart delivers oxygen and nutrients to every part of your body through arteries. You can remember the function of arteries by recalling that "A" stands for "away from the heart." And your heart has to have enough pressure to get that blood down to your fingertips and to the tip of your toes. The arteries will carry blood away from your heart to smaller and smaller blood vessels called capillaries. So when you go to the doctor and they squeeze your fingertips, they are looking at the rate of your capillary refill. Or when you have surgery, you may be asked to remove your fingernail polish or false fingernails. Before, during or after surgery they may check the rate of your capillary refill. It's a form of checking your blood pressure. Capillaries connect the ends of the smallest arteries (arterioles) with the beginnings of the smallest veins (venules) to send the blood back to your heart through the veins. Blood moving back to the heart picks up waste products like a trash truck so that your body can get rid of them. Veins carry the blood back to the heart and it does this against gravity. That's quite a feat when you think about it. So again, there has to be enough pressure generated from the heart in order to get the blood to your fingers and toes, and then back up to the heart again. That's a lot of pressure. Too much or too little pressure can be detrimental to your health. Your Heart is about the size of your clenched fist. And your heart is indeed a muscle. The muscle fibers in the heart are different than the muscle fibers on your legs or that line your organs and blood vessels. This type of muscle fiber is called "cardiac muscle." These muscle fibers branch out and (anastomose) form a continuous network. At intervals, there are prominent bands or intercalated disks that cross the fibers. The special fibers in the heart are called Purkinje fibers. The Purkinje Fibers form the impulse-conducting system of the heart.

Your heart contracts and relaxes approximately 70 or so times a minute at rest. And of course it will contract more when you are exercising. Muscles contract and relax, that's what they do. The heart muscle squeezes and pumps blood through its four chambers to all parts of your body. And it pumps blood through a phenomenal collection of blood vessels. Your blood stream will travel through a pipeline that is very rubbery in nature. This pipeline has tons of branches that are both small and large. When you inhale, you breathe in air and then send it straight down to your lungs. Blood is pumped from the heart to your lungs. This is where oxygen from the air that you've breathed in gets mixed with the blood. The oxygen-rich blood travels back to the heart where it is pumped through your arteries, to the capillaries and to the rest of the whole body. This system delivers oxygen to all the cells in your body. This includes your skin, bones and other organs. Even your bones need blood. Your veins will then carry the oxygen-depleted blood back to the heart for another ride in this huge circulatory system. The majority of your blood is a colorless liquid called plasma. Red blood cells [RBC's] make the blood look red and it's the RBC's that deliver oxygen to the cells in the body and carry back waste gases in exchange. The RBC's look like tiny little inner tubes or donuts under a microscope. In the middle is where the oxygen sits.

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White blood cells [WBC's] are part of your body's defense against disease. Some WBC's will attack and kill germs by devouring them and others will attack and kill by manufacturing and waging chemical warfare agents against disease. Platelets are other cells that help your body repair itself after injury. Platelets play an important role in blood coagulation, hemostasis and blood thrombus formation. When a small vessel is injured, platelets adhere to each other and the edges of the injury and form a plug that covers the area. The plug or blood clot formed soon retracts and stops the loss of blood. BLOOD Blood is considered the essence of life because the uncontrolled loss of it can result to death. Blood is a type of connective tissue, consisting of cells and cell fragments surrounded by a liquid matrix which circulates through the heart and blood vessels. The cells and cell fragments are formed elements and the liquid is plasma. Blood makes about 8% of total weight of the body. Functions of Blood: >transports gases, nutrients, waste products, and hormones >involve in regulation of homeostasis and the maintenance of PH, body temperature, fluid balance, and electrolyte levels >protects against diseases and blood loss PLASMA Plasma is a pale yellow fluid that accounts for over half of the total blood volume. It consists of 92% water and 8% suspended or dissolved substances such as proteins, ions, nutrients, gases, waste products, and regulatory substances. Plasma volume remains relatively constant. Normally, water intake through the GIT closely matches water loss through the kidneys, lungs, GIT and skin. The suspended and dissolved substances come from the liver, kidneys, intestines, endocrine glands, and immune tissues as spleen. FORMED ELEMENTS Cell Type Erythrocytes (RBC) Leukocytes (WBC): Neutrophil Spherical cell, nucleus with two or more lobes connected by thin filaments, cytoplasmic granules stain a light pink or reddish purple, 12-15 micrometers in diameter Spherical cell, nucleus, with two indistinct lobes, cytoplasmic granules stain blue-purple, 10-12 micrometers in diameter Spherical cell, nucleus often bilobed, cytoplasmic granules satin orangered or bright red, 10-12 micrometers in diameter Spherical cell with round nucleus, cytoplasm forms a thin ring around the nucleus, 6-8 micrometers in diameter Phagocytizes microorganism Description Biconcave disk, no nucleus, 7-8 micrometers in diameter Function Transport oxygen and carbon dioxide

Basophil

Releases histamine, which promotes inflammation, and heparin which prevents clot formation Releases chemical that reduce inflammation, attacks certain worm parasites Produces antibodies and other chemicals responsible for destroying microorganisms, responsible for allergic reactions, graft rejection, tumor control, and regulation of the immune system Phagocytic cell in the blood leaves the circulatory system and becomes a macrophage which phagocytises bacteria, dead cells, cell fragments, and debris within tissues Forms platelet plugs, release chemicals necessary for blood clotting

Eosinophil

Lymphocyte

Monocyte Platelet

Spherical or irregular cell, nucleus round or kidney or horse-shoe shaped, contain more cytoplasm than lymphocyte, 10-15 micrometers in diameter Cell fragments surrounded by a cell membrane and containing granules, 2-5 micrometers in diameter

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PREVENTING BLOOD LOSS When a blood vessel is damaged, blood can leak into other tissues and interfere with the normal tissue function or blood can be lost from the body. Small amounts of blood from the body can be tolerated but new blood must be produced to replace the loss blood. If large amounts of blood are lost, death can occur. BLOOD CLOTTING Platelet plugs alone are not sufficient to close large tears or cults in blood vessels. When a blood vessel is severely damaged, blood clotting or coagulation results in the formation of a clot. A clot is a network of threadlike protein fibers called fibrin, which traps blood cells, platelets and fluids. The formation of a blood clot depends on a number of proteins found within plasma called clotting factors. Normally the clotting factors are inactive and do not cause clotting. Following injury however, the clotting factors are activated to produce a clot. This is a complex process involving chemical reactions, but it can be summarized in 3 main stages; the chemical reactions can be stated in two ways: just as with platelets, the contact of inactive clotting factors with exposed connective tissue can result in their activation. Chemicals released from injured tissues can also cause activation of clotting factors. After the initial clotting factors are activated, they in turn activate other clotting factors. A series of reactions results in which each clotting factor activates the next clotting factor in the series until the clotting factor prothrombin activator is formed. Prothrombin activator acts on an inactive clotting factor called prothrombin. Prothrombin is converted to its active form called thrombin. Thrombin converts the inactive clotting factor fibrinogen into its active form, fibrin. The fibrin threads form a network which traps blood cells and platelets and forms the clots. CONTROL OF CLOT FORMATION Without control, clotting would spread from the point of its initiation throughout the entire circulatory system. To prevent unwanted clotting, the blood contains several anticoagulants which prevent clotting factors from forming clots. Normally there are enough anticoagulants in the blood to prevent clot formation. At the injury site, however, the stimulation for activating clotting factors is very strong. So many clotting factors are activated that the anticoagulants no longer can prevent a clot from forming. CLOT RETRACTION AND DISSOLUTION After a clot has formed, it begins to condense into a denser compact structure by a process known as clot retraction. Serum, which is plasma without its clotting factors, is squeezed out of the clot during clot retraction. Consolidation of the clot pulls the edges of the damaged vessels together, helping the stop of the flow of blood, reducing the probability of infection and enhancing healing. The damaged vessel is repaired by the movement of fibroblasts into damaged area and the formation of the new connective tissue. In addition, epithelial cells around the wound divide and fill in the torn area. The clot is dissolved by a process called fibrinolysis. An inactive plasma protein called plasminogen is converted to its active form, which is called plasmin. Thrombin and other clotting factors activated during clot formation, or tissue plasminogen activator released from surrounding tissues, stimulate the conversion of plasminogen to plasmin. Over a period of a few days the plasmin slowly breaks down the fibrin.

NURSING CARE PLAN

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Assessment

Diagnosis

Planning

Implementation

Rationale

Evaluation

S: “Ihi ako ng ihi” - as verbalized by the client O: • • • Frequent urination Dry mucous membrane Weak in appearance

Fluid Volume Deficit related to Active fluid volume loss

After 3 hours of Nursing Intervention The client will maintain fluid volume at a functional level evidence by stable vital signs and moist mucous membrane

1) Increased fluid intake 2) Administered and regulated IV fluids as indicated 3) Monitored Input and Output 4) Administered antidiuretics as ordered

1) To replace the fluid loss 2) To replace fluid loss 3) To see if the interventions are effective 4) Helps control body water balance by reducing urination

Goal met: After 3 hours of nursing interventions the client maintained fluid volume at function level as evidenced by stable vital signs and moist mucous membrane

Assessment

Diagnosis

Planning

Implementation

Rationale

Evaluation

S: “Masakit tang tiyan ko” - as verbalized by the client O: • • (+) facial grimace Guarding the affected part Weak in appearance Pain scale: 8/10

Acute pain related to injuring agent(biological)

After 2 hours of Nursing Intervention The client’s pain will be reduce from 8/10 to 5/10 in the pain scale

1) Assessed pain location, duration and frequency 2) Monitored Vital signs 3) Provided comfort measures 4) Encouraged adequate rest 5) Administered analgesic or antacids as ordered

• •

1) To know where the pain is occurring and its characteristics 2) Usually altered when acute pain is present 3) To provide nonpharmacological treatment 4)To prevent fatigue 5) To meet pain control goals

After 2 hours of Nursing Intervention The patient’s pain was reduced from 8/10 to 5/10 on the pain scale.

Assessment

Diagnosis

Planning

Implementation

Rationale

Evaluation

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S: “Hindi naman masyado mainit ang pakirmdam ko” as verbalized by the client O:

Hyperthermia

Increased body temperature - 37.8oC Warm to touch Weak in appearance

After 2 hours of Nursing Intervention the client’s temperature will be reduce from 37.8o C to 37.2o C

1) Applied Tepid Sponge bath 2) Increased fluid intake 3) Provided high calorie diet 4) Maintained bed rest 5) Administered medications as ordered(antipyretics)

1) To reduce patient’s temperature 2) To prevent dehydration 3) To meet increased metabolic needs 4)To reduce metabolic demands 5) To reduce temperature

After 2 hours of Nursing Intervention the patient’s temperature was reduced from 37.8o C to 37.2o C

Assessment

Diagnosis

Planning

Implementation

Rationale

Evaluation

S: “Hindi ako masyadong makatulog ngayon” as verbalized by the client O:
• Changes in behavior & performance (increasing irritability) temp:37.9oC

Sleep pattern disturb r/t increased body temperature

Within the 8hrs shift of clinical exposure, the SO will: a. verbalize understanding of sleep disturbances b. identify individually appropriate interventions to promote health c. report improvement in sleep/rest pattern

1) Obtained feedback from the patient regarding usual bedtime, routines, number of hours sleepand time of arising. 2) Promoted calm and rested environment 3) Checked and recorded V/S

1) To determine usual sleep pattern and provide comparative baseline 2) To prevent stimulants and to establish optimal slepp/rest patterns 3) To check if there’s a decreased in temperature

Within the 8hrs shift of clinical exposure, goal partially met because the significant others was able to identify some of the interventions to promote good sleep.

DRUG STUDY Drug name Dosage Gen. and specific Indications Specific Side Nursing

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and frequen cy
Genetic: Omeprazole Brand: Lasec 20mg/1ta b OD

classification
General: Antisecretory agent Specific: Proton pump inhibitor • Short-term treatment of active duodenal ulcer First-line therapy in treatment of heartburn or symptoms of gastroesophag eal reflux disease (GERD) Short-term treatment of active benign gastric ulcer GERD, severe erosive esophagitis, poorly responsive symptomatic GERD Long-term therapy: Treatment of pathologic hypersecretory conditions (ZollingerEllison syndrome, multiple adenomas, systemic mastocytosis) Eradication of H. pylori with amoxicillin or metronidazole and clarithromycin Prilosec OTC: Treatment of frequent heartburn (2 or more days per wk) Unlabeled use: Posterior laryngitis; enhance efficacy of pancreatin for the treatment of steatorrhea in cystic fibrosis

action
Gastric acidpump inhibitor: Suppresses gastric acid secretion by specific inhibition of the hydrogenpotassium ATPase enzyme system at the secretory surface of the gastric parietal cells; blocks the final step of acid production.

effects/adverse reaction
CNS: Headache, dizziness, asthenia, vertigo, insomnia, apathy, anxiety, paresthesias, dream abnormalities Dermatologic : Rash, inflammation, urticaria, pruritus, alopecia, dry skin GI: Diarrhea, abdominal pain, nausea, vomiting, constipation, dry mouth, tongue atrophy Respiratory: URI symptoms, cough, epistaxis Other: Cancer in preclinical studies, back pain, fever

responsibilities
Administer before meals. Caution patient to swallow capsules whole—not to open, chew, or crush them. Arrange for further evaluation of patient after 8 wk of therapy for gastroreflux disorders; not intended for maintenanc e therapy. Symptomati c improveme nt does not rule out gastric cancer, which did occur in preclinical studies. Administer antacids with omeprazole , if needed. Take the drug before meals. Swallow the capsules whole; do not chew, open, or crush them. This drug will need to be taken for up to 8 wk (short-term therapy) or for a prolonged period (> 5 yr in some cases). Have regular medical follow-up visits. These side effects may occur: Dizziness (avoid driving or performing hazardous tasks); headache (request medications ); nausea, vomiting, diarrhea (maintain proper nutrition); symptoms

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of upper respiratory tract infection, cough (do not selfmedicate; consult with your health care provider if uncomforta ble). Report severe headache, worsening of symptoms, fever, chills.

Generic: Paracetamol Brand: Acetaminophen

500mg P.O. q 4

Gen.: Antipyretic, Analgesic Specific: Synthetic non-opioid paminophenol derivative

For mild pain and fever

Relieve fever through central action in the hhypothalamic heat regulatin center

Headache Hemolytic anemia Jaundice Rash urticaria

-Tell parents to consult prescriber before giving drug. -Advice patient that drug is only for shortterm use and to consult prescriber - Monitor liver function studies; may cause hepatic toxicity at doses >4g/day - Monitor renal function studies; albumin indicates nephritis - Monitor blood studies, especially CBC and pro-time if patient is on long-term therapy. - Check I&O ratio; decreasing output may indicate renal failure. - Assess for fever and pain - Assess hepatotoxicity: dark urine, claycolored stools - Assess allergic reactions: rash, urticaria

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DISCHARGE PLANS •Instruct patient to take home medication as directed. •Encourage patient to resume daily activities at home. •Advice patient to visit RHU for V/S monitoring and for any untoward symptoms observed. •Instruct patient to maintain proper hygiene like taking a bath everyday. •Instruct to come back after a week at OPD for follow up check-up. •Instruct patient to eat foods rich in iron like green leafy vegetables and organ meats, also to increase oral fluid intake. •Encourage patient to go to mass and pray regularly.

HEALTH TEACHING GUIDE

DATE & VENUE Health teaching will be held at the Medical ward.

OBJECTIVES

LEARNING CONTENTS The following are the contents of the teaching: 1. Use mosquito netting around your bed. 2. Limit the amount the exposed skin by wearing pants and long-sleeved shirts. Cover up as much as you can, even wearing socks and boots. 3. Be sure to remove all standing water that makes perfect breeding grounds for the mosquito. 4. Apply mosquito repellant

STRATEGIES

TARGET

RESOURCES

EVALUATION

EXPECTED OUTCOME The client was able to do following after an hour: 1. Demonstrate the proper cleaning of the environment 2. Verbalize plan to eliminate health and safety hazards. 3. Demonstrate appropriate, effective use of resources.

After an hour of health teaching the client will be able: 1. Demonstrate the proper cleaning of the environment 2. Verbalize plan to eliminate health and safety hazards. 3. Demonstrate appropriate, effective use of resources.

- lecture discussion - learning interaction - demonstration

The target of this teaching plan is the client.

- Internet - - time and effort of the student

The following questions will be ask to the patient: 1. What will you apply on the skin to prevent mosquito bites? 2. what will you place around your bed to prevent mosquito bites? 3. what will you remove to prevent the breeding of the mosquitoes.

Some Advice on Preventing and Dealing with Viral Infections There are several ways to prevent infection and the transmission of germs. These useful tips can help you to remain healthy and develop a stronger immune system: • • • • Maintain a healthy lifestyle by eating properly, obtaining sufficient rest and exercising regularly. Wash your hands frequently and thoroughly – before cooking, eating or after visiting the toilet. Avoid contact with someone who has an illness that you may catch such as a cold, the flu, chickenpox, or measles. Avoid touching your eyes or nose if you have been in contact with someone who has a cold.

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• • • • • • • • • • •

Practice good personal hygiene by showering or bathing everyday, washing your hair, and trimming your nails regularly. Brush and floss your teeth twice a day, and visit your dentist regularly to prevent infection and cavities. Use cleaning detergents and rubber gloves when cleaning your home Pop sponges and dish cloths into the microwave to disinfect them, as they harbor the most germs. Cover your mouth when you cough or sneeze. Do not eat or drink while working with contaminated things or while cleaning up. Practice safe sex. Using condoms during sexual intercourse will reduce the spread of sexually transmitted diseases. Eat protein and cooked vegetables at least twice a day as this helps to rebuild the immune system. Drink bottled or filtered water as it is less likely to be contaminated. Increase your intake of nutritional supplements to prevent infections by helping to eliminate toxic substances, improve digestion, and balance body chemistry. Positive attitudes and healthy emotions also strengthen the immune system and help you to live longer and feel younger and healthier.

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