Case Study of SVI

ASSESSMENT
A. General Information
Client’s initials: GEG Rm/Wd: Isolation Room (Medical Ward) Date Admitted: Aug. 24, 2009
Age: 28 Sex: Male OS: Single Nat. Filipino Race: Malay Rel. Roman Catholic
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 Beats/min R 25 cpm

BP: 100/70 mm Hg Weight 65 kg Ht. 5’8
Allergies none
Medications: none
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.
1.6 History of illness in the family:

• (-) HPN
• (+) OM- Paternal Side
2. NUTRITION AND METABOLIC PATTERN

2.1 Usual food (before admission)
•Breakfast - rice, egg, fried foods, water
•Lunch - rice, soup, water, vegetables
•Supper - rice, paksiw, water
•Snacks - 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.
Preferences: He preferred to drink coffee than soft drinks.

2.3 Any food restrictions:
- My client doesn’t have any food restrictions.
2.4 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)
- 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.
C. Physical Assessment
Date Performed: August 26, 2009
V/S:
BP= 120/80 mm Hg PR= 68 bpm
RR= 18 cpm Temp= 37.8oC
General Appearance:
- Conscious and coherent
- 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 Normal Findings Actual Findings Remarks

Used
SKIN
Color and pigmentation Inspection Light to deep brown Light to deep brown Normal
Lesions Inspection No lesions, scars or No lesions, Scar is due to a
inflammation inflammation, have a minor operation
scar on the left thumb
Texture Palpation Smooth and even Smooth and even Normal
Moisture Palpation Moist Moist Normal
Temperature Palpation Warm Hot Hyperthermia
Mobility and Turgor Palpation Skin pinches easily Skin pinches easily Normal
and immediately and immediately
returns to its original returns to its original
position. position.
NAILS
Nail bed color Inspection Pink Pink Normal
Shape Inspection Convex Convex Normal
Lesions Inspection No inflammation of No inflammation of Normal
the skin around the the skin around the
nail nail
Texture Palpation Hard and immobile Hard and immobile Normal
Capillary refill Palpation Pink tone returns Pink tone returns Normal
immediately to immediately to
blanched nailbeds blanched nailbeds
when pressure is when pressure is
released. released.
HEAD
Size Inspection Proportion to the Proportion to the Normal
body and the skull is body and the skull is
rounded and smooth rounded and smooth
Symmetry Inspection Symmetrical Symmetrical Normal
HAIR Inspection Black Black Normal

Color Inspection Straight and short Straight and short Normal
Texture Inspection No nits/lice present No nits/lice present Normal
Other Findings
SCALP
Distribution of hair Inspection Evenly distributed Evenly distributed Normal
Lesions Inspection No inflammation, No inflammation, Normal
lumps or masses lumps or masses
Other Findings Inspection Absence of seborrhea Absence of seborrhea Normal
FACE
Skin color Inspection Light to deep brown Light to deep brown Normal
Texture Inspection Smooth Smooth Normal
Facial movement Inspection Symmetric facial Symmetric facial Normal
movement movement
EYES
External structure Inspection Evenly distributed, Evenly distributed, Normal
pupil is round, black pupil is round, black
and 2-3 mm in size, and 2-3 mm in size,
iris are brown, iris are brown,
symmetrical and symmetrical and
there no signs of there no signs of
lesions and markings lesions and markings
Eyebrows Inspection Evenly distributed Evenly distributed Normal
Eyelashes Inspection Equally aligned Equally aligned Normal
Eyelids Inspection Evenly distributed, Evenly distributed, Normal
curved outward curved outward
Conjunctiva Inspection Pink Pink Normal
Pupillary reflexes Inspection Constrict when the Constrict when the Normal
light reflexed, pupils light reflexed, pupils
are equally round and are equally round and
reactive to light and reactive to light and
acccomodation acccomodation
EARS
Color Inspection Same as facial color Same as facial color Normal
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Symmetry Inspection Symmetrical at the Symmetrical at the Normal
level of the eyes level of the eyes
corner corner
Shape and size Inspection Symmetric to head Symmetric to head Normal
Canal discharge Inspection No discharges and No discharges and Normal
inflammation inflammation
NOSE
Color Inspection Same as facial color Same as facial color Normal
Shape Inspection Symmetric Symmetric Normal
Discharges Inspection No discharges No discharges Normal
MOUTH
Symmetry Inspection Symmetric Symmetric Normal
Color Inspection Pink Pink Normal
Moisture Palpation Moist Moist Normal
TONGUE
Position Inspection Positioned at the Positioned at the Normal
center, can move center, can move
freely freely
Color Inspection Dull red Dull red Normal
Texture Inspection Smooth Smooth Normal
Mobility Inspection Can move freely Can move freely Normal
Lesions Inspection No lesions or No lesions or Normal
Gums Inspection No lesion and no No lesion and no Normal
signs of bleeding signs of bleeding
Teeth Inspection No cavities No cavities Normal
Tonsils Inspection No swelling, able to No swelling, able to Normal

swallow swallow
NECK
Position Inspection Head centered Head centered Normal
Range of movements Inspection Smooth movements Smooth movements Normal
without discomfort without discomfort
Palpation Symmetric and at Symmetric and at Normal
midline position midline position
Lymph nodes Palpation No swelling, No swelling, Normal
enlargement, and enlargement, and
tenderness tenderness
Thyroid gland Inspection Landmarks are Landmarks are Normal
and Palpation positioned at midline. positioned at midline.
No masses or No masses or
tenderness. tenderness.
THORAX
Chest Inspection Symmetrical chest Symmetrical chest Normal
expansion expansion
Palpation No tenderness No tenderness Normal
Lungs Auscultation No adventitious No adventitious Normal
sound sound
UPPER EXTREMITIES
Size Inspection Equal size Equal size Normal
Lesions Inspection No lesions, No lesions, Normal
deformities or deformities or
Musculoskeletal functions Inspection No pain when No pain when Normal
moving, negative for moving, negative for
masses and masses and
Brachial and radial arteries Inspection Equal strength Equal strength Normal
bilaterally bilaterally Normal
CHEST
Breasts and axillae Inspection Flat and no Flat and no Normal
dimplings, axillae dimplings, axillae
doesn’t have a rash or doesn’t have a rash or
infection noted infection noted
Thorax Inspection Symmetric with ribs Symmetric with ribs Normal
sloping downward at sloping downward at
approximately 45oC approximately 45oC
degree angle in degree angle in
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relation to the spine relation to the spine
Precordium Palpation No pulsations or No pulsations or Normal
vibration vibration
Neck veins Auscultation No blowing or No blowing or Normal
swishing swishing
ABDOMINAL
4 Abdominal quadrants Palpation Nontender and Nontender and Normal
soft,no guarding and soft,no guarding and
masses masses
Liver Palpation Not palpable Not palpable Normal
Spleen Palpation Not palpable Not palpable Normal
Kidneys Palpation Not palpable Not palpable Normal
LOWER EXTREMITIES
Size Inspection Equal size Equal size Normal
Lesions Inspection No lesions, No lesions, Normal
deformities or deformities or
Musculoskeletal function Inspection No pain when No pain when Normal
moving, negative for moving, negative for
masses and masses and
Popliteal, posterior tibia and pedal Inspection strong and equal Srong and equal Normal
arteries bilaterally bilaterally
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 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.
RESPIRATORY SYSTEM Because of the increase cardiac output cause by bleeding the
patient respiration also increase to supply enough oxygen to the
body organs and cells.
ENDOCRINE SYSTEM 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 NORMAL FINDINGS ACTUAL FINDINGS ANALYSIS

Hematocrit M: 0.40-0.54 0.48 Normal
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Platelet Count 150-450 x 10^g/L 163 x 10^g/dL Normal
URINALYSIS REPORT

Color Yellow Amber Yellow Normal
Transparency Clear to slightly turbid clear Normal
Reaction 4.5-8 6.5 Normal
Specific Gravity 1.005-1.030 1.005 Normal
Sugar Negative Negative Normal
Protein Negative Negative Normal
Squamous Epithelial Cells Few Occasional Normal
Red Blood Cells Few 0-2 Normal
Pus Cells Few 0-2 Normal
HEMATOLOGY REPORT
Time: 6:30PM

Hemoglobin M: 130-180 g/dL 136 g/dL Normal
Hematocrit M: 0.40-0.54 .52 Normal
Lymphocytes 0.20-0.30 0.42 Increased due to the
body’s increased immune
system
HEMATOLOGY REPORT

Hemoglobin M: 130-180 g/dL 154 g/dL Normal
Hematocrit M: 0.40-0.54 .51 Normal
SEROLOGY REPORT
TEST NORMAL FINDINGS RESULT REMARK

Typhidot Negative lgG Negative
Typhidot Negative lgM Negative
Abnormal Findings;
• Lymphocytes- 0.42 d/t the body’s increased immune system
INTRAVENOUS FLOW SHEET
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Date Solution Time started Amount to follow
8-24-09
3-11 #1 D5LR1Lx30gtts/min 1600H PLR1Lx40gtts/min
#2 PLRx40gtts/min 2200H #3PLRx40gtts/min
11-7 #3 PLRx40gtts/min 0600H #4 PLRx40gtts/min
8-25-09

8-26-09
I & O MONITORING
Shift Oral Urine
8-24-09
3-11 500cc 450cc
8-25-09
7-3 500cc 480cc
3-11 600cc 1200cc
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 (+) Heat production
(vasoconstriction, behavior changes) (involuntary muscle contractions)
FEVER
When treated early with doctor When illness become severe

prescribed medications and managed
to prevent the appearance of other
symptoms.
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 in

rashes 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 community-
associated 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 high-
impact 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. SARS-
CoV 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 mannose-
binding 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 SARS-
CoV 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 cox-
sackieadenovirus 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
Page | 13
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
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,
Typical bacteria, pain will occur at the site of the
body aches etc. They can be local at times as in
symptoms 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.
Page | 14
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.
Page | 15
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.
Page | 16
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 life-
threatening 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.
Page | 17
REVIEW OF ANATOMY AND PHYSIOLOGY
CARDIOVASCULAR SYSTEM
Page | 18
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 Description Function

Erythrocytes (RBC) Biconcave disk, no nucleus, 7-8 Transport oxygen and carbon
micrometers in diameter dioxide
Leukocytes (WBC):
Neutrophil Spherical cell, nucleus with two or Phagocytizes microorganism

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

Basophil indistinct lobes, cytoplasmic Releases histamine, which promotes
granules stain blue-purple, 10-12 inflammation, and heparin which
micrometers in diameter prevents clot formation
Spherical cell, nucleus often bilobed,

cytoplasmic granules satin orange- Releases chemical that reduce
Eosinophil red or bright red, 10-12 micrometers inflammation, attacks certain worm
in diameter parasites
Spherical cell with round nucleus,

cytoplasm forms a thin ring around Produces antibodies and other
Lymphocyte the nucleus, 6-8 micrometers in chemicals responsible for destroying
diameter microorganisms, responsible for
allergic reactions, graft rejection,
tumor control, and regulation of the
immune system
Spherical or irregular cell, nucleus Phagocytic cell in the blood leaves

round or kidney or horse-shoe the circulatory system and becomes
Monocyte shaped, contain more cytoplasm than a macrophage which phagocytises
lymphocyte, 10-15 micrometers in bacteria, dead cells, cell fragments,
diameter and debris within tissues
Platelet Cell fragments surrounded by a cell Forms platelet plugs, release
membrane and containing granules, chemicals necessary for blood
2-5 micrometers in diameter clotting
Page | 20
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
Page | 21
Assessment Diagnosis Planning Implementation Rationale Evaluation
S: “Ihi ako ng ihi” Fluid Volume After 3 hours of 1) Increased fluid 1) To replace the Goal met:
- as verbalized by the Deficit Nursing intake fluid loss After 3 hours of
client related to Intervention 2) Administered and 2) To replace nursing
Active fluid The client will regulated IV fluids as fluid loss interventions the
O: volume loss maintain fluid indicated 3) To see if the client maintained
• Frequent volume at a 3) Monitored Input interventions are fluid volume at
urination functional level and Output effective function level as
evidence by 4) Administered 4) Helps control evidenced by
• Dry mucous stable vital signs antidiuretics as body water stable vital signs
membrane and moist ordered balance by and moist mucous
mucous reducing membrane
• Weak in membrane urination
appearance
S: “Masakit tang Acute pain After 2 hours of 1) Assessed pain 1) To know After 2 hours of
tiyan ko” - as related to Nursing location, duration and where the pain is Nursing
verbalized by the injuring Intervention frequency occurring and its Intervention
client agent(biologi- The client’s characteristics The patient’s
cal) pain will be 2) Monitored Vital 2) Usually pain was reduced
O: reduce from signs altered when from 8/10 to 5/10
• (+) facial 8/10 to 5/10 in acute pain is on the pain scale.
grimace the pain scale present
3) Provided comfort 3) To provide
• Guarding measures non-
the affected pharmacological
part treatment
4) Encouraged 4)To prevent
• Weak in adequate rest fatigue
appearance 5) Administered 5) To meet pain
analgesic or antacids control goals
• Pain scale: as ordered
8/10
Page | 22
S: “Hindi naman Hyperthermia After 2 hours of 1) Applied Tepid 1) To reduce After 2 hours of
masyado mainit ang Nursing Sponge bath patient’s Nursing
pakirmdam ko” as Intervention the temperature Intervention the
verbalized by the client’s 2) Increased fluid 2) To prevent patient’s
client temperature will intake dehydration temperature was
be reduce from 3) Provided high 3) To meet reduced from
O: 37.8o C to 37.2o calorie diet increased 37.8o C to 37.2o
• Increased C metabolic needs C
body 4) Maintained bed 4)To reduce
temperature rest metabolic
- 37.8oC demands
5) Administered 5) To reduce
medications as temperature
• Warm to ordered(antipyretics)
touch
• Weak in
appearance
S: “Hindi ako Sleep pattern Within the 8hrs 1) Obtained feedback 1) To determine Within the 8hrs
masyadong disturb r/t shift of clinical from the patient usual sleep shift of clinical
makatulog ngayon” increased body exposure, the SO regarding usual pattern and exposure, goal
as verbalized by the temperature will: bedtime, routines, provide partially met
client a. verbalize number of hours comparative because the
understanding of sleepand time of baseline significant others
O: sleep arising. was able to
• Changes in disturbances 2) Promoted calm 2) To prevent identify some of
behavior & b. identify and rested stimulants and to the interventions
performance individually environment establish optimal to promote good
(increasing appropriate slepp/rest sleep.
irritability)
interventions to patterns
promote health 3) Checked and 3) To check if
• temp:37.9oC
c. report recorded V/S there’s a
improvement in decreased in
sleep/rest pattern temperature
DRUG STUDY
Drug name Dosage Gen. and specific Indications Specific Side Nursing
Page | 23
and classification action effects/adverse responsibilities
frequen reaction
cy
Genetic: 20mg/1ta General: • Short-term Gastric acid- CNS: - Administer
Omeprazole b Antisecretory agent treatment of pump Headache, before
Brand: Lasec OD Specific: Proton active inhibitor: dizziness, meals.
pump inhibitor duodenal ulcer Suppresses asthenia, Caution
gastric acid vertigo, patient to
• First-line secretion by insomnia, swallow
therapy in specific apathy, capsules
treatment of inhibition of anxiety, whole—not
heartburn or the hydrogen- paresthesias, to open,
symptoms of potassium dream chew, or
gastroesophag ATPase abnormalities crush them.
eal reflux enzyme Dermatologic
disease system at the : Rash, - Arrange for
(GERD) secretory inflammation, further
surface of the urticaria, evaluation
• Short-term gastric parietal pruritus, of patient
treatment of cells; blocks alopecia, dry after 8 wk
active benign the final step skin of therapy
gastric ulcer of acid GI: Diarrhea, for
production. abdominal gastroreflux
pain, nausea, disorders;
• GERD, severe vomiting, not
erosive constipation, intended for
esophagitis, dry mouth, maintenanc
poorly tongue e therapy.
responsive atrophy Symptomati
symptomatic Respiratory: c
GERD URI improveme
symptoms, nt does not
• Long-term cough, rule out
therapy: epistaxis gastric
Treatment of Other: cancer,
pathologic Cancer in which did
hypersecretory preclinical occur in
conditions studies, back preclinical
(Zollinger- pain, fever studies.
Ellison
syndrome, - Administer
multiple antacids
adenomas, with
systemic omeprazole
mastocytosis) , if needed.
• Eradication of - Take the

H. pylori with drug before
amoxicillin or meals.
metronidazole Swallow
and the capsules
clarithromycin whole; do
not chew,
open, or
• Prilosec OTC:
crush them.
Treatment of This drug
frequent will need to
heartburn (2 be taken for
or more days up to 8 wk
per wk) (short-term
therapy) or
• Unlabeled for a
use: Posterior prolonged
laryngitis; period (> 5
enhance yr in some
efficacy of cases).
pancreatin for
the treatment - Have
of steatorrhea regular
in cystic medical
fibrosis 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
Page | 24
of upper
respiratory
tract
infection,
cough (do
not self-
medicate;
consult
with your
health care
provider if
uncomforta
ble).
- Report
severe
headache,
worsening
of
symptoms,
fever,
chills.
Generic: 500mg Gen.: Antipyretic, For mild pain and fever Relieve fever Headache -Tell parents to
Paracetamol P.O. q 4 Analgesic through Hemolytic anemia consult prescriber
Specific: Synthetic central action Jaundice before giving drug.
Brand: non-opioid p- in the Rash -Advice patient that
Acetaminophen aminophenol hhypothalamic urticaria drug is only for short-
derivative heat regulatin term use and to consult
center 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, clay-
colored stools
- Assess allergic
reactions: rash,
urticaria
Page | 25
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 OBJECTIVES LEARNING STRATEGIES TARGET RESOURCES EVALUATION EXPECTED

& CONTENTS OUTCOME
VENUE
Health After an hour of The following - lecture The target - Internet The following The client was
teaching health teaching are the discussion of this - - time and questions will be able to do
will be the client will be contents of the - learning teaching effort of the ask to the patient: following after
held at able: teaching: interaction plan is the student 1. What will you an hour:
the 1. Demonstrate 1. Use - demonstration client. apply on the skin 1. Demonstrate
Medical the proper mosquito to prevent the proper
ward. cleaning of the netting around mosquito bites? cleaning of the
environment your bed. 2. what will you environment
2. Verbalize plan 2. Limit the place around your 2. Verbalize
to eliminate amount the bed to prevent plan to
health and safety exposed skin mosquito bites? eliminate health
hazards. by wearing 3. what will you and safety
3. Demonstrate pants and remove to prevent hazards.
appropriate, long-sleeved the breeding of 3. Demonstrate
effective use of shirts. Cover the mosquitoes. appropriate,
resources. up as much as effective use of
you can, even resources.
wearing socks
and boots.
3. Be sure to
remove all
standing water
that makes
perfect
breeding
grounds for
the mosquito.
4. Apply
mosquito
repellant
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.
Page | 26
• 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.
Page | 27

Case Study of SVI

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ASSESSMENT

Admitting VS: T 37.9oC P 75 bpm Beats/min R 25 cpm

B. Nursing History (Based on the Functional Health Pattern by Gordon)

1.5 History of hospitalization (when, where, and why)

1.6 History of illness in the family:

• (+) OM- Paternal Side

2. NUTRITION AND METABOLIC PATTERN

•Lunch - rice, soup, water, vegetables

•Supper - rice, paksiw, water

•Type of Diet: no dark foods

•Mouth condition: moist and pink

Preferences: My client preferred to eat vegetable and dishes with soup.

Preferences: He preferred to drink coffee than soft drinks.

2.4 Any problems with ability to eat:

Complaints of usual pattern of bowel movement: none

3.3 Skin: (condition)

- c IVF on R of PLRS 1L@350mL/0800Hx40gtts/min

4. ACTIVITY EXERCISE PATTERN

6.2 Ability to read and write. Any difficulty in learning

7.2 Present health goals

7.3 Appearance: calm, comfortable, appropriate dress and hygiene

8.3 Significant person to client:

8.4 Complaints regarding family:

10. COPING-STRESS MANAGEMENT PATTERN

10.2 Any significant stress in the past year

10.3 Management of stress

11. VALUE BELIEF SYSTEM

11.2 Importance of God to client:

11.3 Religious practices (type and frequency):

12. DEVELOPMENTAL TASKS (Assess for achievement of development tasks)

- Smooth and steady gait; stands firm and erect

- No destructive mannerism or involuntary movements

Area assessed Technique Normal Findings Actual Findings Remarks

HAIR Inspection Black Black Normal

Tonsils Inspection No swelling, able to No swelling, able to Normal

Summary of Abnormal Findings:

PARAMETER NORMAL FINDINGS ACTUAL FINDINGS ANALYSIS

PARAMETER NORMAL FINDINGS ACTUAL FINDINGS ANALYSIS

PARAMETER NORMAL FINDINGS ACTUAL FINDINGS ANALYSIS

PARAMETER NORMAL FINDINGS ACTUAL FINDINGS ANALYSIS

TEST NORMAL FINDINGS RESULT REMARK

INTRAVENOUS FLOW SHEET

3-11 #4 PLRx40gtts/min 1210H #5 PLRx40gtts/min

Infects cells and generate cellular response

Cytokines destroys cell membrane and cell wall

Elevated thermoregulatory set-point

When treated early with doctor When illness become severe

Damage cell due to both cytokines

IVF’s and Electrolytes replacement

Fluid shift from ICF-ECF

Manifest evanescent Rashes in

Bloody vomitus, urine, and stool

DATA FROM THE TEXTBOOK

Respiratory syncytial virus

Severe acute respiratory distress syndrome

Viral hemorrhagic fevers

Comparison of viral and bacterial infection

Characteristic Viral Bacterial

The classic symptoms of a bacterial infection are

Cause Pathogenic viruses Pathogenic bacteria

What Causes Viral Infections?

Help for Viral Infections

• Over-the-counter painkillers and anti-inflammatories such as paracetamol or ibuprofen can reduce

Natural Herbal and Homeopathic Remedies for Viral Infection