DENGUE
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OUTLINE
Definition
Anatomy & Physiology
Etiology
Symptomatology
Pathophysiology
Management
a. Diagnostic Exams & Laboratory
Tests
b. Pharmacological Management
c. Therapeutic Management
d. Surgical Management
e. Nursing Management
DEFINITION
Dengue virus has become a looming threat
across the globe due to its dramatic rise in
reported cases, possessing the ability to cause
a spectrum of illnesses, ranging from mild fever
to life-threatening complications, especially in
young children. The Aedes aegypti mosquito,
the primary culprit behind the spread of this
mosquito-borne
virus
called
Flavivirus,
transmits four distinct serotypes: DENV-1,
DENV-2, DENV-3, and DENV-4. These
serotypes contribute to the complexity of
Dengue, as they can cause varying degrees of
illness. Clinical presentations can range from a
self-limiting, mild fever to a more severe form
known as Dengue Hemorrhagic Fever (DHF),
characterized by hemorrhagic manifestations
and shock. The geographic distribution of the
Dengue virus largely overlaps with the
ecological niche of the Aedes aegypti mosquito,
encompassing tropical and subtropical regions.
These regions face a constant threat of Dengue
fever outbreaks, highlighting the critical need
for effective prevention and control strategies.
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ANATOMY & PHYSIOLOGY
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Cardiovascular System – The exact
pathophysiology that leads to cardiac
involvement in dengue infection are unknown.
However, two mechanisms of cardiac injury are
presented. The first involves DENV directly
invading and damaging cardiac myocytes,
while the second involves cytokine-induced
myocardial cell injury caused by ongoing
inflammation. Clinical manifestations of dengue
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virus-induced cardiac complications range from
self-limiting arrhythmias to severe myocardial
infarction with hypotension, pulmonary edema,
and cardiogenic shock.
Blood and Blood Vessels – Dengue infection
significantly affects the blood and blood
vessels, leading to plasma leakage, activation
of the hemostatic system, and increased
platelet activation. These complications can
lead to severe outcomes, such as shock and
death, and can impact the blood supply, with
increased demand for platelets and fresh frozen
plasma.
Skin –DENV first encounters human cells
through the skin. The majority of patients with
fever caused by Dengue viral illness develop a
distinctive rash. The rash is transient, flushing,
and erythemic in nature, caused by capillary
dilation. Mobiliform or maculopapular eruptions
are common and usually asymptomatic. This
rash may be pruritic in a small percentage of
patients. Hemorrhagic manifestations such as
petechiae and mucosal membrane bleeding are
also possible.
Musculoskeletal System – Patients with DVI
may exhibit muscle involvement in the form of
myalgias, myositis, rhabdomyolysis, and
hypokalemic paralysis. DENV has the ability to
infect and modify the calcium storage of
skeletal muscle cells. This finding supports the
hypothesis that skeletal muscle dysfunction
during DVI is caused by DENV infection of
skeletal muscle fibers.
Nervous System – The mechanisms of
neurological involvements during DVI are
thought to be related to the specific type of
neurological disease. However, viral and host
factors play critical roles in disease
pathogenesis. Neuropathogenesis could be
attributed to direct viral invasion of the CNS,
autoimmune
reactions,
and
metabolic
disturbances or alterations. The most common
cranial symptoms are severe headaches and
retro-orbital eye pain. Pathologies can cause
retro-orbital eye pain. The most commonly
accepted cause is thrombocytopenia-related
ophthalmic bleeding. Bleeding in the macula
and retinal periphery may cause retro-orbital
pain.
GI System – Dengue virus also causes
intestinal mucosal ischemia, as evidenced by
an increase in serum intestinal fatty acid
binding proteins.
etiology of dengue is essential for efficient
disease treatment and designing treatment
approaches. If left untreated, it can lead to
hemorrhagic fever or dengue shock syndrome,
leading to organ dysfunction and potentially
fatal outcomes.
ETIOLOGY
PREDISPOSING FACTORS
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Age
Geographical location
Economic status
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PRECIPITATING FACTORS
Prior dengue infection
Poor vector control
Recent travel history
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SYMPTOMATOLOGY
High fever
Skin rash
Severe headache
Retro-orbital pain
Vomiting
Muscle pain
Bone pain
Joint pain
Fatigue
Bleeding
Severe abdominal pain
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PATHOPHYSIOLOGY
The disease progression of Dengue fever
typically initiates with predisposing and
precipitating factors outlined in its etiology.
These factors contribute to the presence of the
Aedes mosquito vector, primarily Aedes
aegypti, which is the primary transmitter of
DENV. When an infected mosquito bites a
human host, it injects the dengue virus into the
host’s skin through its proboscis. Upon biting,
the mosquito’s saliva containing DENV will be
deposited into the epidermis or dermis layers of
the skin. After which, the dengue virus settles in
the epidermal cells of the skin, where it begins
to interact with the host’s immune system.
Dengue fever is a disease caused by the entry
of the Dengue virus into the skin by Langerhans
cells, which release antigen-specific receptors.
This entry allows the virus to enter cells and
spread through endocytosis, causing the
release of viral RNA and replication. The virus
then infects the body's reticuloendothelial
system, leading to systemic infection. This can
cause symptoms such as muscle, bone, joint
pain, fatigue, gastrointestinal conditions, and
blood cell destruction. The immune response is
activated, releasing pyrogens, fever, headache,
nausea, vomiting, lymphadenopathy, and
increased vascular permeability. Dengue fever
can be classified into categories like dengue
without warning signs, dengue with warning
signs, and severe dengue. Immediate and
appropriate management is crucial to reduce
death and morbidity. Understanding the
MANAGEMENT
DIAGNOSTIC EXAMS & LABORATORY TESTS
• CBC
• IgM Antibody Enzyme-linked Immunosorbent
Assay (MAC-ELISA)
• Nucleic Acid Amplification Test - LoopMediated Isothermal Amplification Assay
(NAAT-LAMP)
• Dengue NS1 RDT or Dengue Nonstructural
protein 1 (NS1) Rapid Diagnostic Test (RDT)
• Plaque Reduction Neutralization Test (PRNT)
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PHARMACOLOGICAL MANAGEMENT
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Acetaminophen
Dengue tetravalent vaccine
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THERAPEUTIC MANAGEMENT
IV Therapy
Electrolyte therapy or oral rehydration therapy
Blood transfusion
Complete bed rest
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SURGICAL MANAGEMENT
Surgical intervention in dengue patients is risky
due to potential complications like bleeding and
organ damage. However, in severe cases
where surgery is absolutely necessary, it
should be carefully considered and reserved for
patients with specific complications like
gallbladder
inflammation,
pancreas
inflammation, appendix inflammation, spleen
injury, bowel tears, internal bleeding, or blood
clots. Instead of surgery, less invasive methods
like
draining
abscesses
or
using
angioembolization to stop spleen bleeding
should be thought about. For simpler cases like
mild gallbladder or appendix issues, nonsurgical treatments are preferred. Decisions
about care and whether to do invasive
procedures should be made case by case by a
team of experts, including doctors, surgeons,
critical care specialists, radiologists, and
anesthetists.
NURSING MANAGEMENT
Risk for bleeding
o Goal: The Client will be able to
demonstrate behaviors that reduce the
risk of bleeding.
Risk for fluid volume deficit
o Goal: Client will be able to maintain
adequate
hydration
status
as
evidenced by good skin turgor and oral
mucous membranes, balanced fluid
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intake and output, and stable vital
signs.
Acute pain
o Goal: The patient will have better wellbeing, as evidenced by baseline pulse,
blood pressure, and breathing levels.
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SCHISTOSOMIASIS
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IV.
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VI.
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OUTLINE
Definition
Anatomy & Physiology
Etiology
Symptomatology
Pathophysiology
Management
a. Diagnostic Exams & Laboratory
Tests
b. Pharmacological Management
c. Therapeutic Management
d. Surgical Management
e. Nursing Management
DEFINITION
Schistosomiasis, known as bilharzia, is an
acute and chronic parasitic infection with blood
flukes (trematode worms) of the genus
Schistosoma (E.g., S. mansoni, S. mekongi, S.
intercalatum, and S. japonicum and S.
haematobium)
acquired
through
skin
penetration by swimming or often walking in
contaminated freshwater with the larval forms
(cercariae) of schistosomes. It is prevalent in
tropical and subtropical areas, such as
impoverished communities with poor sanitation
and lack of access to clean drinking water. It
affects the blood vessels of the gastrointestinal
or genitourinary system of the infected person.
ANATOMY & PHYSIOLOGY
Gastrointestinal System – As for a patient
with schistosomiasis, chronic inflammation and
tissue damage occur due to the presence of
Schistosoma eggs in the intestinal wall. This
leads to the formation of granulomas and
fibrosis, resulting in thickening and scarring of
the intestinal wall. Severe inflammation may
lead to ulceration of the intestinal mucosa,
causing symptoms such as abdominal pain and
bloody diarrhea. Abnormal tissue growths, such
as polyps or pseudopolyps, may form within the
intestines due to chronic inflammation and
repair processes. The intestinal mucosa may
undergo hypertrophy and hyperplasia in
response to the presence of Schistosoma
parasites and their eggs. Fibrosis and scarring
can result in the narrowing of the intestinal
lumen, leading to strictures that may cause
obstruction
and
other
complications.
Schistosomiasis can also affect other organs,
particularly the liver, leading to complications
such as periportal fibrosis.
Urinary bladder – Therefore, schistosomiasis
not only impairs the normal function of the
urinary bladder by causing inflammation and
structural damage but also poses a long-term
risk of severe complications, including cancer,
underscoring the importance of early diagnosis
and effective treatment of this parasitic disease.
ETIOLOGY
PREDISPOSING FACTORS
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Age
People living in tropical and subtropical regions
near contaminated/infested water
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PRECIPITATING FACTORS
Poor sanitation
Lack of access to potable drinking water
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SYMPTOMATOLOGY
Itchy, red, and blotchy rash
Fever
Dry cough
Muscle aches & pain
Stomach pain
Hepatomegaly
Hematuria
Iron-deficiency anemia
Hematochezia
Colonic polyps
Intestinal mucosal ulcerations
Bleeding
Scar tissue formation
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PATHOPHYSIOLOGY
Schistosomiasis is a parasitic disease caused
by trematode worms of the genus Schistosoma,
primarily transmitted through contact with
contaminated freshwater. Five Schistosoma
species, including Schistosoma haematobium,
mansoni,
japonicum,
mekongi,
and
intercalatum, infect the urinary tract, intestine,
and liver. The disease is primarily transmitted
through contact with contaminated freshwater,
with most cases occurring in tropical and
subtropical regions. The disease is transmitted
through contact with contaminated freshwater,
with most cases occurring in people swimming
or bathing in contaminated water. The disease
can cause systemic hypersensitivity reactions,
pulmonary
symptoms,
muscle
aches,
abdominal pain, hepatomegaly, bladder
involvement, iron-deficiency anemia, and
ulceration in the bladder wall. The adult worms
travel to their final home in small veins in the
bladder or intestine, where they live an average
of 3 to 10 years. The disease is a significant
public health concern in tropical and subtropical
regions, particularly in Africa, Asia, and South
America.
MANAGEMENT
DIAGNOSTIC EXAMS & LABORATORY TESTS
• Stool sample
• Urine sample
• PCR Assay
• Blood test
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Kato-Katz Technique
Biopsy
Falcon Assay Screening Test - Enzyme-linked
Immunosorbent Assay (FAST-ELISA
Point-of-Care Circulating Cathodic Antigen
(POC-CCA) Cassette Test
Circum Ova Precipitin Test (COPT)
PHARMACOLOGICAL MANAGEMENT
• Praziquantel
• Oxamniquine
• Niridazole
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THERAPEUTIC MANAGEMENT
Maintaining Good Personal Hygiene
Avoid Contact with Contaminated Water
Snail Control
Environmental Sanitation
Access to Clean Water Sources
Increased fluid intake
SURGICAL MANAGEMENT
Endoscopic Variceal Ligation (EVL) for
Hepatosplenic Schistosomiasis
Transurethral
Resection
(Severe/Chronic
Schistosomiasis Infection)
NURSING MANAGEMENT
Impaired
Tissue
Integrity
related
to
inflammatory response secondary to parasitic
infection, as evidenced by lesions and ulcers of
affected tissues.
o Goal: The client will be able to
demonstrate specific behaviors and
make lifestyle adjustments that are
critical for the healing of lesions and
ulcers, and to prevent further infection.
Acute Pain related to inflammation as
evidenced by abdominal pain, cramping, and
pain during urination, with a reported pain level
of 8 out of 10 pain scale.
o Goal: The client will report a pain level
reduced to 3 out of 10 pain scale, as a
result of effective pain management
strategies.
Risk for Impaired Urinary Elimination related to
urinary tract involvement and potential kidney
damage
o Goal: The client will be able to
demonstrate behaviors to reduce risk
factors and improve elimination
pattern.
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LEPTOSPIROSIS
I.
II.
III.
IV.
V.
VI.
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OUTLINE
Definition
Anatomy & Physiology
Etiology
Symptomatology
Pathophysiology
Management
a. Diagnostic Exams & Laboratory
Tests
b. Pharmacological Management
c. Therapeutic Management
d. Surgical Management
e. Nursing Management
DEFINITION
Leptospirosis is a bacterial disease that affects
humans and animals. It is caused by bacteria of
the genus Leptospira. In humans, it can cause
a wide range of symptoms, some of which may
be mistaken for other diseases. Some infected
persons, however, may have no symptoms at
all. Without treatment, Leptospirosis can lead to
kidney damage, meningitis (inflammation of the
membrane around the brain and spinal cord),
liver failure, respiratory distress, and even
death (CDC, 2019).
Human infections are acquired by direct contact
with infected urine or tissue or indirectly by
contact with contaminated water or soil.
Abraded
skin
and
exposed
mucous
membranes (conjunctival, nasal, oral) are the
usual entry portals. Leptospirosis can be an
occupational disease (eg, of farmers or sewer
and abattoir workers), but in the US, most
patients are exposed incidentally during
recreational activities (eg, swimming in
contaminated fresh water). Outbreaks have
been reported outside the US after heavy
rainfall or freshwater flooding. Leptospira can
survive for several weeks to months in
freshwater sources (eg, lakes, ponds).
However, they can survive for only a few hours
in salt water (Nazir et.al., 2023).
ANATOMY & PHYSIOLOGY
Renal system - In the renal system,
leptospirosis often leads to acute kidney injury
(AKI) due to direct damage to the renal tubules
and glomeruli. The infection triggers an
inflammatory
response,
causing
tubulointerstitial nephritis, which impairs the
kidneys' ability to filter waste products and
regulate electrolyte balance. As a result,
individuals with leptospirosis commonly present
with symptoms such as oliguria, proteinuria,
and elevated serum creatinine levels. If left
untreated, severe cases can progress to kidney
failure.
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Nervous system – The bacteria can invade the
central nervous system (CNS) through the
bloodstream or via direct extension from nearby
tissues. Once in the CNS, leptospires trigger an
inflammatory response, resulting in meningitis,
which is inflammation of the membranes
surrounding the brain and spinal cord. This
inflammation can cause symptoms such as
severe headache, neck stiffness, photophobia,
and altered mental status. In more severe
cases,
leptospirosis
can
lead
to
meningoencephalitis, involving inflammation of
the brain itself, which may manifest as seizures,
confusion, and focal neurological deficits.
Hepatic system – This hepatic involvement is
primarily due to the bacteria's ability to directly
damage hepatocytes and trigger an immune
response within the liver. As a result, individuals
with leptospirosis often present with symptoms
such as jaundice (yellowing of the skin and
eyes), abdominal pain, and elevated liver
enzymes. Severe cases may progress to acute
liver failure, characterized by coagulopathy,
hepatic encephalopathy, and multi-organ
dysfunction syndrome.
Musculoskeletal system – Once in the
muscles, leptospires trigger an inflammatory
response, resulting in myositis, characterized
by muscle pain, tenderness, and weakness.
This inflammatory process can lead to muscle
fiber damage and the release of muscle
enzymes into the bloodstream, causing
elevated creatine kinase levels. Additionally,
leptospirosis may cause severe muscle
involvement, such as rhabdomyolysis, a
potentially
life-threatening
condition
characterized by the rapid breakdown of
skeletal muscle tissue.
ETIOLOGY
PREDISPOSING FACTORS
Leptospira bacteria
PRECIPITATING FACTORS
Occupation
Outdoor activities
Exposure to infected animals
Tropical climates
Presence of cut or wound in the skin
Heavy rainfall and flooding
Poor hygiene practices (Unsafe drinking water,
contact with contaminated soil)
SYMPTOMATOLOGY
Headache
Severe muscular ache
High Fever
Chills
Jaundice
Red eyes
Nausea and Vomiting
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Rash
Meningitis
Iridocyclitis
Optic neuritis
Peripheral neuropathy
Renal failure
PATHOPHYSIOLOGY
Leptospirosis is an acute bacterial septicemic
febrile disease caused by pathogenic species
of Leptospira, affecting humans and animals
worldwide. It has a biphasic clinical
presentation, beginning with the septicemic
phase followed by immune manifestations. The
Weil syndrome is the most severe form,
causing multisystem damage. Transmission
can occur through skin abrasions, mucous
membranes, soil, contaminated water, and
urine of infected animals. Leptospires colonize
reservoirs,
causing
morphological
and
immunoenzymatic changes. The liver is a major
target organ, with pathology reports showing
congested sinusoids and distention of the
space of Disse. Leptospires migrate to the
kidneys, causing interstitial nephritis and
tubular necrosis. Renal failure can be rapid due
to tubular damage or hypovolemia. If
suspected, antimicrobial therapy should be
initiated immediately. Mild symptoms may
require doxycycline, while severe cases may
require hospitalization and supportive therapy.
Survivors generally experience little long-term
morbidity, with hepatic and renal functions
returning to normal.
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SURGICAL MANAGEMENT
There is no surgical procedures indicated for
leptospirosis.
NURSING MANAGEMENT
Acute pain
o Goal: To manifest pain reduction
intensity to a manageable level (2-3) on
a standardized pain scale of 0 to 10.
Risk for deficient fluid volume
o Goal: To maintain adequate fluid
volume
Hyperthermia
o Goal: To maintain core body
temperature within normal range
MANAGEMENT
DIAGNOSTIC EXAMS & LABORATORY TESTS
• Dark-field Microscopy
• Biliary tract ultrasonography
• Chest X-ray
• Magnetic Resonance Imaging
• Complete Blood Count
• Urinalysis
• Polymerase Chain Reaction Test
• Microscopic Agglutination Testing
• Enzyme-linked Immunosorbent Assay
• Immunohistochemistry
• CSF Analysis
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PHARMACOLOGICAL MANAGEMENT
Doxycycline
Azithromycin
Penicillin G
Ceftriaxone
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THERAPEUTIC MANAGEMENT
Ventilatory support
Renal replacement therapy (Hemodialysis)
Intravenous fluid therapy
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DENGUE
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IV.
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VI.
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OUTLINE
Definition
Anatomy & Physiology
Etiology
Symptomatology
Pathophysiology
Management
a. Diagnostic Exams & Laboratory
Tests
b. Pharmacological Management
c. Therapeutic Management
d. Surgical Management
e. Nursing Management
DEFINITION
Rabies is a viral disease that affects the central
nervous system of humans and other
mammals. It is caused by the Rabies virus, a
member of the Lyssavirus genus. In humans,
rabies can lead to a variety of symptoms, which
often progress rapidly and can include fever,
headache, anxiety, hallucinations, paralysis,
and, eventually, death if not treated promptly
(CDC, 2020).
The transmission of rabies to humans typically
occurs through the bite or scratch of an infected
animal, with dogs being the most common
source
worldwide.
Other
sources
of
transmission include bats, raccoons, skunks,
and foxes. The virus is present in the saliva of
infected animals, and transmission can also
occur if the saliva comes into contact with
mucous membranes or open wounds.
ANATOMY & PHYSIOLOGY
Nervous system – In the context of rabies, the
virus primarily targets the nervous system,
infecting and causing inflammation in the brain
and spinal cord, leading to the characteristic
neurological symptoms associated with the
disease (Alberts, B., et. al., 2019).
Brain – In the context of rabies, the virus
primarily targets the brain, leading to acute
inflammation and encephalitis. This viral
invasion of the brain disrupts its normal
function, causing the characteristic symptoms
of rabies, such as confusion, hallucinations,
and eventually, coma and death if not treated
promptly (Kandel, E.R., et. al., 2018).
Spinal cord – In the context of rabies infection,
the spinal cord becomes a target for the virus,
which can lead to inflammation, demyelination,
and neuronal damage, disrupting its normal
functions and causing severe neurological
symptoms (Marieb, E.N., & Hoehn, K., 2019).
Peripheral Nerve – The rabies virus enters the
body through a bite or scratch from an infected
animal. The virus then travels through
peripheral nerves, likely using specific
receptors on the nerve cells, towards the
central nervous system. Once it reaches the
CNS, the virus infects nerve cells in the brain
and spinal cord, causing the characteristic
symptoms of rabies like disorientation,
aggression, and paralysis. This progressive
damage to the nervous system ultimately leads
to death (Matsumoto, K., & Ogawa, T., 2020).
ETIOLOGY
PREDISPOSING FACTORS
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Age
Exposure to infected animals
PRECIPITATING FACTORS
Improper Wound Care
Failure to receive Post-Exposure Prophylaxis
(PEP)
Failure to Quarantine Suspect Rabid Animals
Outdoor Activities
SYMPTOMATOLOGY
IN HUMANS
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Fever
Neurological
Dysfunction
Hyperactivity (Furious Rabies)
Paralytic Rabies
Hydrophobia
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IN ANIMALS
Unprovoked Abnormal Aggression
Hypersalivation
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PATHOPHYSIOLOGY
Rabies is a fatal viral disease affecting the
central nervous system caused by the highly
neurotrophic rabies virus. It is spread through
bites, scratches, wounds, mucosal exposure,
and in rare cases, transplanted CNS tissues.
Rabies is a vaccine-preventable disease that
can be treated before or after exposure. To
protect against canine rabies, deep muscle
inoculation is required. The virus takes a long
time to incubate and spreads along the
neuromuscular junction, causing symptoms
such as pain, fever, and flu-like illness. The
virus then spreads to the spinal cord and brain
tissue, leading to rapidly progressing
encephalitis. The clinical course of rabies can
be divided into two phases: prodromal phase
and acute neurologic phase. The prodromal
phase begins with fever and flu-like symptoms,
while the acute neurologic phase is associated
with objective signs of developing brain
damage. Rabies is a vaccine-preventable
disease, but it is crucial to get vaccinated as
soon as possible after exposure to avoid its fatal
course.
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MANAGEMENT
DIAGNOSTIC EXAMS & LABORATORY TESTS
• Direct Fluorescent Antibody (DFA) Test
• Immunohistochemistry (IHC)
• Rapid Rabies Enzyme Immunodiagnosis
(RREID)
• Magnetic Resonance Imaging (MRI)
• Lumbar Puncture Virus Isolation
• Polymerase Chain Reaction Test
PHARMACOLOGICAL MANAGEMENT
• Rabies Virus Strain Flury Lep Antigen
• Rabies Immune Globulin (Human)
• Tetanus Toxoid
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THERAPEUTIC MANAGEMENT
IV Therapy
O2 therapy
SURGICAL MANAGEMENT
Surgical intervention is generally not
recommended for the management of rabies.
NURSING MANAGEMENT
Risk for injury
o Goal: At the end of the nursing
interventions, the patient will remain
free from any injury.
Impaired skin integrity
o At the end of nursing interventions, the
patient will be able to Prevent infection
and promote wound healing.
Disturbed thought process
o Goal: At the end of nursing
interventions, the patient maintains a
normal thought process & cognition by
exhibiting normal behaviour and
absence of mood changes.
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