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Hemorrhagic Fever
II
Submitted By:
Wincy S. Banayad
Submitted To:
Dengue Hemorrhagic fever is a wide spread disease in our country. This is brought
about by a mosquito called Aedes Aegypti, which dwells in any clean stagnant water.
This case study, aims to provide knowledge to the possible treatment or any medical
management that can be done in a patient who is infected by this vector borne illness
Objectives:
Patient’s History: Five (5) days PTC, Patient was noted to have a moderate to
high Grade fever, this was accompanied by Abdominal Pain
and Headache. Self medication was done ( paracetamol and
bioflu ). The above condition persisted. No consultation was
done till there is an episode of nose bleeding, this lead to a
consultation into a lyin – in clinic.
Clinical History: Five (5) days PTA, Patient have High Grade Fever
One (1) day PTA, persistent High Grade Fever
and Abdominal Pain. Consulted into a private M.D.
When a mosquito carrying DENV bites a person, the virus enters the skin together
with the mosquito's saliva. It binds to and enters white blood cells, and reproduces
inside the cells while they move throughout the body. The white blood cells respond
by producing a number of signalling proteins (such as interferon) that are responsble
for many of the symptoms, such as the fever, the flu-like symptoms and the severe
pains. In severe infection, the virus production inside the body is much increased, and
many more organs (such as the liver and the bone marrow) can be affected, and fluid
from the bloodstream leaks through the wall of small blood vessels into body cavities.
As a result, less blood circulates in the blood vessels, and the blood pressure becomes
so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction
of the bone marrow leads to reduced numbers of platelets, which are necessary for
effective blood clotting; this increases the risk of bleeding, the other major
complication of dengue.
After entering the skin, DENV binds to Langerhans cells (a population of dendritic
cells in the skin that identifies pathogens).The virus enters the cells through binding
between viral proteins and membrane proteins on the Langerhans cell, specifically the
C-type lectins called DC-SIGN, mannose receptor and CLEC5A.DC-SIGN, a non-
specific receptor for foreign material on dendritic cells, seems to be the main one. The
dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is
replicated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the
cell's protein synthesis apparatus produces new viral proteins, and the viral RNA is
copied. Immature virus particles are transported to the Golgi apparatus, the part of the
cell where the some of the proteins receive necessarily sugar chains (glycoproteins).
The now mature new viruses bud on the surface of the infected cell and are released
by exocytosis. They are then able enter other white blood cells (such as monocytes
and macrophages).
The initial reaction of infected cells is to produce the interferon, a cytokine that raises
a number of defenses against viral infection through the innate immune system by
augmenting the production of a large group of proteins (mediated by the JAK-STAT
pathway). Some serotypes of DENV appear to have mechanisms to slow down this
process. Interferon also activates the adaptive immune system, which leads to the
generation of antibodies against the virus as well as T cells that directly attack any
cell infected with the virus.Various antibodies are generated; some bind closely to the
viral proteins and target them for phagocytosis (ingestion by specialized cells) and
destruction, but some bind the virus less well and appear instead to deliver the virus
into a part of the phagocytes where it is not destroyed but is able to replicate further.
Dengue virus
Dengue (DF) and dengue hemorrhagic fever (DHF) are caused by one of four closely
related, but antigenically distinct, virus serotypes (DEN-1, DEN-2, DEN-3,
and DEN-4), of the genus Flavivirus.
Immunity
Infection with one of these serotypes provides immunity to only that serotype for life,
so persons living in a dengueendemic area can have more than one dengue infection
during their lifetime. If an individual develops immunity to one subtype and then tries
to launch an immune response to another subtype then they will develop DHF/DSS.
Work has been done on a tetravalent vaccine that will attempt to give the individual
immunity to all four of the subtypes at the same time.
Mechanism of complications
It is useful to understand why certain individual develop DHF/DSS. The Dengue
virus has been shown to have 4 subtypes. These 4 subtypes are different strains of
dengue virus that have 60-80% homology between each other. The major difference
for humans lies in subtle differences in the surface proteins of the different dengue
subtypes. After a person is infected with dengue, he or she develops an immune
response to that dengue subtype. The immune response produces specific antibodies
to that subtype's surface proteins that prevent the virus from binding to macrophage
cells (the target cell that dengue viruses infect) and gaining entry. However, if another
subtype of dengue virus infects the individual, the virus will activate the
immune system to attack it as if it was the first subtype. The immune system is tricked
because the 4 subtypes have very similar surface antigens. The antibodies bind to the
surface proteins but do not inactivate the virus. The immune response attracts
numerous macrophages, which the virus proceeds to infect because it has not been
inactivated. This situation is referred to as Antibody-Dependent Enhancement (ADE)
of a viral infection. This makes the viral infection much more acute. The body
releases cytokines that cause the endothelial tissue to become permeable
which results in hemorrhage and plasma loss from the blood vessels. Increased
vascular permeability leads to plasma loss from the vascular compartment. This
results in haemoconcentration, low pulse pressure. When the plasma loss becomes
critical, shock ensues. Both quantitative and qualitative platelet defects can develop.
Therefore bleeding time can be prolonged even when platelet counts are above
100,000 per cubic millimeter. In the liver there is focal necrosis of hepatocytes,
swelling, appearance of Councilman bodies and hyaline necrosis of
Kupffer cells.
Anatomy and Physiology: The circulatory system composed of the heart and blood
vessels that moves blood into the entire body system is
the one affected in this illness. During a DHF, the
severe type of dengue, this is characterized by high
fever, serious hemorrhage, pneu. Which may lead to
shock
Medical Management:
Dengue fever is usually a self-limited illness, and only supportive care is required.
Acetaminophen may be used to treat patients with symptomatic fever. Aspirin,
nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids should be
avoided.
• Patients with known or suspected dengue fever should have their platelet count
and hematocrit measured daily from the third day of illness until 1-2 days after
defervescencePatients who do not improve should be admitted to the hospital
for continued hydration.
• Patients who develop signs of dengue hemorrhagic fever warrant closer
observation. Thus, require admission for intravenous fluid administration.
• Successful management of severe dengue requires careful attention to fluid
management and proactive treatment of hemorrhage. Patients with internal or
gastrointestinal bleeding may require transfusion. Patients with coagulopathy
may require fresh frozen plasma.
• After patients with dehydration are stabilized, they usually require intravenous
fluids for no more than 24-48 hours. Intravenous fluids should be stopped
when the hematocrit level falls below 40% and adequate intravascular volume
is present. Patients who are resuscitated from shock rapidly recover. Patients
with dengue hemorrhagic fever or dengue shock syndrome may be discharged
from the hospital when they meet the following criteria:
• Afebrile for 24 hours without antipyretics
• Good appetite, clinically improved condition
• Adequate urine output
• Stable hematocrit level
• At least 48 hours since recovery from shock
• Absence of respiratory distress
• Platelet count greater than 50,000 cells/μL
Consultations
Consultation with an infectious diseases specialist may be helpful in guiding
decisions regarding diagnosis and treatment.
Consultation with a critical care medicine specialist may be helpful when
treating patients with dengue hemorrhagic fever or dengue shock syndrome
and severe hemorrhagic manifestations or shock.
Diet
No specific diet is necessary for patients with dengue fever, but the EDCF diet
is most preferably.
Patients may become dehydrated from fever, lack of oral intake, or vomiting.
Patients who are able to tolerate oral fluids should be encouraged to drink oral
rehydration solution, fruit juice, or water to prevent dehydration.
Return of appetite after dengue hemorrhagic fever or dengue shock syndrome
is a sign of recovery.
Activity
Bedrest is recommended for patients with symptomatic dengue fever, dengue
hemorrhagic fever, or dengue shock syndrome.
Assessment Diagnosis Planning Intervention Rationale Evaluation
On bed most of
the time