Dengue Hemorrhagic Fever

DENGUE HEMORRHAGIC FEVER
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3.1. Dengue Fever
3.1.1. Definition
Dengue fever is the most common fever in the age group of children, adolescents
and adults. In general, dengue fever is an acute febrile condition, which sometimes has a
biphasic pattern and is accompanied by severe headaches, myalgias, arthralgias, skin
rashes, leukopenia and thrombocytopenia. Even though dengue fever is actually a harmless
condition, it can cause sufferers to be unable to do activities due to severe headaches,
muscle, joint and bone pain (break-bone fever), especially in adults. Sometimes atypical
bleeding occurs, such as gastrointestinal bleeding, hypermenorrhea, and massive epistaxis.
In areas experiencing dengue fever epidemics, transmission of dengue fever rarely occurs
between local residents
Dengue hemorrhagic fever (DHF) is more common in children under 15 years of

age in hyperendemic areas, and it is associated with recurrent dengue infection. However,
its incidence in adults is also increasing. DHF is characterized by a high fever with an
acute onset with symptoms and signs similar to the symptoms and signs of dengue fever in
the initial phase. In DHF, abnormalities in bleeding can be found, for example, a positive
tourniquet (rumple leed) test, petechiae, bruises and gastrointestinal bleeding in more
severe cases.
At the end of the febrile phase, there is a threat of hypovolemic shock (dengue
shock syndrome) due to plasma leakage. The emergence of warning signs such as
persistent vomiting, abdominal pain, lethargy, restlessness, irritability, and oliguria is an
important thing to be followed up immediately in order to prevent shock. Hemostatic
disorders and plasma leakage are the main pathophysiological processes in DHF.
Thrombocytopenia and increased hematocrit/hemoconcentration are features that are
invariably encountered before a reduction in fever/onset of shock. DHF mostly occurs in
children who get a second infection with the dengue virus. There are also reports of DHF
cases occurring in the first infections with DENV-1 and DENV-3 viruses as well as
infections in infants. 6
Expanded dengue syndrome is an unusual manifestation that is increasingly being

reported in cases of dengue hemorrhagic fever and dengue fever where there is
involvement of organs such as the liver, kidneys, brain and heart which are related to
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dengue infection, but there is no evidence of plasma leakage. This may be caused by co-
infection, co-morbidity, or complications from prolonged shock. A more in-depth study
needs to be done for this case. Most patients with dengue hemorrhagic fever who
experience this unusual manifestation are caused by prolonged shock accompanied by
organ failure
Undifferentiated fever Undifferentiated fever is a fever in infants, children and adults

caused by dengue virus infection, especially if the infection is the first time it occurs
(primary dengue infection) where this fever cannot be distinguished from fever due to
other viral infections. A maculopapular rash may accompany fever or as the fever returns
to normal. Other symptoms that often accompany are symptoms involving the respiratory
and gastrointestinal systems
3.1.2. Etiology
Dengue virus types 1, 2, 3 and 4 (group Arthropod borne virus group B) are
transmitted through the bite of many Aedes mosquito species (among others Aedes aegypti
and Aedes albopi. Four different dengue viruses are known to cause dengue fever. Dengue
fever occurs when a person is bitten by a mosquito infected with the virus. The Aedes
aegypti mosquito is the main species that spreads the disease. There are over 100 million
new cases of dengue fever every year worldwide. A small number of these develop into
dengue fever.7
Most infections in the United States are brought in from other countries. Risk
factors for dengue include having antibodies to the dengue virus from a previous infection
(Vyas, et al, 2014). Dengue virus belongs to the genus Flavirus, family flaviridae, there are
4 serotypes of the virus with DEN-1, DEN-2, DEN-3 and DEN-4, all four of which are
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found in Indonesia with the most den-3 serotypes. Infection with one serotype will produce
antibodies against the serotype in question, while the antibodies formed against the other
serotypes are very lacking, so they cannot provide adequate protection against other
serotypes. A person living in the epidermal area of dengue can be infected by 3 or 4
serotypes during his life. The four serotypes of dengue virus can be found in various
regions in Indonesia.6
3.1.3. Symptom
Clinical features Dengue fever After an incubation period of an average of 4-6
days (range, 3-16 days), various non-specific constitutional symptoms as well as
headache, back pain and malaise begin to appear. The uniqueness of the onset of dengue
fever is fever that rises suddenly with a sharp increase in temperature and is often
accompanied by facial flushing and headache. Occasionally, chills accompany a sudden
rise in temperature. After that, retro-orbital pain can appear which is especially felt when
moving the eyeball or if pressure is applied to the eyeball, photophobia, back pain,
muscle pain and bone/joint pain. Other symptoms that often appear are anorexia and
changes in tongue taste sensation, constipation, colicky abdominal pain. groin area pain,
sore throat and depression. These symptoms usually persist for several days to several
weeks. It is important to note that the symptoms of dengue fever vary widely in terms of
frequency and severity
Fever: body temperature usually ranges from 39 oC - 40 oC, fever has a biphasic
pattern, and lasts 5-7 days in most cases.
Skin rash: a diffuse rash of short duration appearing on the face, neck and chest in
the first 2 to 3 days; later, a marked rash appears as maculopapular or rubelliform lesions
on the 3rd and 4th day. At the end of the feverish period, or as soon as the temperature
begins to drop, the diffuse rash will disappear, and clusters of localized petechiae will
appear in such locations as the soles of the feet, feet, palms and arms. This healing rash has
the characteristic, namely, scattered petechiae between the surrounding areas of pale, and
normal surrounding skin. 11. Itchiness in the rash can be found
Bleeding manifestations: skin bleeding may be seen as a positive tourniquet test

and/or petechiae. Other bleeding such as massive epistaxis, hypermenorrhea and
gastrointestinal bleeding rarely occur in DD which is exacerbated by thrombocytopenia.
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Disease course: the duration and severity of DD varies between individuals in each
epidemic area. The recovery phase may be reached in a short time and without serious
problems but sometimes it is also often ongoing. In adults, it sometimes lasts for several
weeks and may be accompanied by asthenia and depression. Bradycardia often occurs
during the healing phase. Bleeding due to complications of DF, such as epistaxis, bleeding
gums, gastrointestinal bleeding, hematuria and hypermenorrhoea, is rare. However, heavy
bleeding (DD with unusual bleeding) is an important cause of death in DF. Dengue fever
with bleeding manifestations must be differentiated from dengue hemorrhagic fever
3.1.4. Illness Course

A. Dengue infection course
Dengue is an infection with complex manifestations with an incubation period of
4 to 10 days, and has 3 phases in the course of the disease, namely the febrile phase,
the critical phase, and the recovery phase (Figure 2). Accuracy and speed of
management as well as patient monitoring since the febrile phase, can reduce the risk
of death in severe dengue patients to <0.5%
Figure 2. The course of dengue infection.

Source: Yip WCL. Dengue haemorrhagic fever: Current
approaches to management. Medical
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1. Fever Phase
The febrile phase is characterized by sudden
onset of high fever (can reach 40oC), continuous,
sometimes biphasic, and lasts 2–7 days. Fever is
accompanied by other common symptoms such as
facial flushing, headache, retroorbital pain, anorexia,
myalgia, and arthralgia. Other symptoms that may be
encountered are heartburn, nausea, vomiting, pain in
the right subcostal area or diffuse abdominal pain,
sometimes accompanied by sore throat. Redness of
the pharynx and conjunctiva (pharyngeal injection
and ciliary injection) may be found on physical
examination. In the early febrile phase, it is difficult
to distinguish clinically dengue from other non-
dengue febrile illnesses. A differential diagnosis is
deemed necessary so that appropriate management
can be carried out.
Table 1. Differential Diagnosis of Dengue in the Fever Phase
Dengue-like condition in the Fever Phase

Flue like syndrome Colds, influenza, measles, chikungunya, infections
mononucleosis, COVID-19, HIV seroconversion
Fever and rash Rubella, measles, fever scarlatina,
infection
meningococci, chikungunya, drug reactions
Diarrhea Rotavirus, another intestinal infection
Disease with Meningoencephalitis, febrile seizures
neurological manifestations
Source: WHO. Dengue guidelines for diagnosis, treatment
and control, 2009.
Mild bleeding manifestations such as

petechiae and bleeding of the mucous membranes (eg
epistaxis and bleeding gums) may occur. Changes in
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the results of a complete peripheral blood count
during the febrile phase in the form of a progressive
decrease in the number of leukocytes (leukopenia)
can guide clinicians to diagnose dengue. In dengue
infection the total number of leukocytes, neutrophils
and platelets is lower when compared to patients with
fever caused by other viruses in dengue endemic
areas.
2. Critical Phase
The critical phase occurs when the fever

drops (time of fever defervescence), that is, when the
body temperature drops to 37.5–38o C or less and
remains below that temperature. This is when plasma
leakage occurs so that the patient can experience
hypovolemic shock. This symptom marks the
beginning of the critical phase. Danger signs
generally occur towards the end of the febrile phase,
namely between the 3rd to 7th day of illness, in the
form of increased capillary permeability together
with an increase in hematocrit levels. Periods of
significant plasma leakage usually last 24–48 hours.
The appearance of warning signs is a

sign of worsening that needs to be watched out for.
The presence of a warning sign is a risk factor for
severe dengue. Most patients will experience
improvement after defervescence. Although rare,
there are patients who go into a critical phase even
shock without defervescence.
In these patients there was a very rapid increase

in hematocrit. In these circumstances, changes in
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blood test results become very important in
determining the onset of the critical phase.
Table 2. Differential diagnosis of dengue in the critical phase
Dengue-like condition in Critical Phase

Infectious Acute gastroenteritis, malaria, leptospirosis, typhoid fever, typhus, viral
disease hepatitis, acute HIV seroconversion, bacterial sepsis, septic shock, COVID-
19
Malignancy Acute leukemia and other malignancies
Other Acute abdomen:
clinical - acute appendicitis
symptoms
- acute cholecystitis
- intestinal
perforation Diabetic
ketoacidosis Lactic
acidosis Blood
disorders Renal
disorders
and control, 2009
Warning signsgenerally occurs towards the end of the

febrile phase between the 3rd to 7th day of illness, in the
form of increased capillary permeability together with an
increase in hematocrit levels. Warning signs are signs of
worsening dengue that need to be watched out for
Every time you find a patient with fever with

suspicion of dengue, it is necessary to do a serial
examination of the peripheral blood. The presence of
progressive leukopenia followed by a rapid decrease in the
number of platelets generally precedes plasma leakage. The
presence of severe plasma leakage (pleural effusion, ascites,
hemoconcentration, hypoalbumin and hypoproteinemia) is a
risk for shock. The patient's clinical condition worsened as
indicated by the presence of warning signs, referred to as
dengue with warning signs (Table 3).
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Most cases of dengue with warning signs will
improve with early intravenous fluids, although some may
develop severe dengue.
Setting clear definitions for warning signs and the severity

of dengue infection is important to avoid unnecessary
hospitalization, especially during an outbreak.
Table 3. Warning signs
Parameter Description Explanation

Clinical Throw up Keep going-continuously ≥3 episodes of vomiting within 12 hours
(persistent) and no
can tolerate oral fluids
Pain or tenderness Abdominal pain is continuous and intensity
Abdomen increased to interfere with activity
Restless/lethargic decreased consciousness and/or irritability
Mucosal bleeding 1) nosebleed/epistaxis
2) gum bleeding
3) petechial skin bleeding
4) purpura
5)bleeding in the conjunctiva,
subconjunctiva
Hepatomegaly >2cm An enlarged liver is palpable on
examination
physical > 2cm
Clinical found palpebral edema, pleural effusion, ascites
fluid accumulation
Laboratory Hematocrit level and platelet count Enhancement hematocrit
comparedearlier,
accompanied by a rapid decline in
numbers
thrombocyte.
Source: Morra ME, et al. Definitions for warning signs and
signs of severe dengue according to the WHO 2009
classification: Systematic review of literature. Rev Med
Virol. 2018 Jul;28(4):e1979.
Pleural effusion and ascites can be detected

clinically depending on the level of plasma leakage
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and volume. Chest X-ray examination (especially the
right lateral decubitus position) and abdominal
ultrasonography are useful adjuncts for diagnosis.
The degree of increase in the hematocrit level above
normal often indicates the severity of plasma leakage.
Persistent vomiting and severe abdominal pain

are early signs of plasma leakage, and may worsen or
persist when the patient is in shock. The patient
appears increasingly lethargic, but generally remains
conscious. Spontaneous mucosal bleeding or bleeding
at the site of blood collection is an important and
common bleeding manifestation. Hepatomegaly and
abdominal pain are also common. The findings of
signs and symptoms that are more severe than the
warning signs in (Table 3), indicate the condition and
classification of the patient as severe dengue.
3. Recovery Phase
If the patient survives the critical phase within

24–48 hours, reabsorption of extravascular fluid will
gradually occur over the next 48–72 hours. General
condition improves, appetite improves,
gastrointestinal symptoms disappear, hemodynamic
status stabilizes, followed by improvement in
diuresis. Some patients show signs of "white isles in
the sea of red", some may experience pruritus.
Bradycardia and electrocardiographic changes are
common in the recovery phase. The hematocrit will
be stable or lower than normal due to the dilution
effect of fluid absorption. The leukocyte count begins
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to increase soon after defervescence whereas the
platelet count returns to normal afterward.
is redundantly rendered in Figure 3.
Figure 3. Clinical problems during the dengue disease course

Source: WHO. Dengue guidelines for diagnosis, treatment and
control, 2009.
3.1.5 Classification of Dengue Infection
A prospective multicenter clinical study in a

WHO/TDR-supported dengue endemic area pooled
evidence to establish criteria for classifying dengue
according to severity. The study findings confirm that
using a single set of clinical and/or laboratory parameters
can assess a clear difference between patients with severe
and non-severe dengue. However, for practical reasons,
the group of patients with non-severe dengue was divided
into two subgroups
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namely dengue patients with warning signs and
without warning signs, for this reason the classification
of dengue diagnosis is as follows (Figure 4)11:
a) Dengue without warning signs.

b) Dengue with warning signs.
c) Severedengue.
Figure 4. Classification of Dengue Infection

Source: WHO. Dengue guidelines for
diagnosis, treatment and control, 2009.
Dengue severity classification can be used practically

by doctors in determining management, how closely patients
need to be monitored during triage and hospitalization, for
more consistent reporting on a national and international
scale, and as a final step in vaccine trials and drug research.
Dengue patients without warning signs may develop severe
dengue. Comorbid factors in patients with dengue infection
allow the condition of dengue without warning signs to
progress to warning signs or severe dengue.
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1. SevereDengue
Severe dengue cases in Southeast Asia occupy

the highest place, namely 15% of all severe dengue
cases. Among the severe cases of dengue, 244 (90%)
had plasma leakage, 39 (14%) severe bleeding, and 28
(10%) severe organ dysfunction. The highest frequency
of plasma seepage occurs in the age group <15 years.
Severe dengue is defined as one or more of the
following conditions, (a) plasma leakage causing shock
(dengue shock) and/or accumulation of liquid
with/without respiratory distress, and/or(b) heavy
bleeding (c) severe organ damage
Increased vascular permeability is followed by severe

hypovolemia until shock occurs, occurring during
defervescence. Early in shock, compensatory
mechanisms occur to maintain a normal systolic
pressure, causing tachycardia and peripheral
vasoconstriction. At this time the diastolic pressure
increases so that the pulse pressure narrows followed
by an increase in peripheral resistance. Dengue patients
who are in shock will remain conscious. At the end of
shock, decompensation will occur, namely systolic and
diastolic pressure will drop suddenly. Prolonged
hypotensive shock and hypoxia can trigger multi-organ
failure which is a very complex clinical condition, for
this reason it is necessary to evaluate the
presence/absence of a process of hemodynamic
changes by assessing the patient's condition as a whole.
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Table 4. Hemodynamic assessment: the process of hemodynamic changes
Parameter Circulati Compensated Shock Decompensated

on Shock
Stable
Level of Contact OK, Good contact, normal Inadequate contact,
conscious responsenormal response to voice only responds to pain
ness (alerts) response (pain) until
nocompletely
unresponsive to
stimulus
(unresponsive)
Time Fast (<2 Slow (>2 seconds) Very slow, kutis
capillary seconds) marmorata
filling
Extremity Warm Cold peripheral Extremity
extremities and
pink moistand cold
Volume Good volume Weak, fast, and Weak or non-existent
peripheral Shallow
pulse
Heart Normal Tachycardia Tachycardia
rate according to age heavy with
bradycardia
15
in further shock
Blood Normal blood Normal systolic pressure Narrow pulse pressure
pressure pressure for but increased diastolic (<20mmHg)
age pressure Hypotension*
pulse
narrowed
Parameter Circulation Compensated Decompensated

Stable Shock Shock
Pressure Postural Blood pressure is not
hypotension detected
pulsenormally fit
age
Breathing Frequency Tachypnea Acidosis metabolic/
frequency breath hyperpnea/Kussmaul
breathing
normalaccording to
age
Diuresis Normal There is a Anuria
 For BB patient decrease in
<30 kgs diuresis from
hence diuresis normal values
1
ml/kgbb/hour m
 For BB
patient 30
kg hence
diuresis
0.5
ml/kgbb/hour
Explanation of the normal values of

respiratory rate, heart rate and blood pressure in the
age group of infants and children:
Age Normal Normal Normal Normal MAP

(lower limit)
breath rate heart rate systolic BP
(upper limit) (upper limit) (lower limit)
1 month 35 (55) 120 (175) 60 (50) 45 (35)
1 year 30 (40) 110 (170) 80 (70) 55 (40)
2 years 25 (30) 100 (160) 90+2*age# 55+ 1.5* age#
(70+ 2* ages)# (40+1.5* ages)#
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6 years 20 (25) 90 (130) 90+2*age# 55+ 1.5* age#
(70+ 2* ages)# (40+1.5* ages)#
12 years 15 (20) 80 (100) 120 (90) 80 (65)
old
Source: European Pediatric Advanced Life Support. ERC Guidelines
2015 edition.
To recognize shock, when examining patients with

dengue infection, it is enough for health workers to simply
hold the patient's hand for 30 seconds to assess
hemodynamics in the form of adequacy of peripheral
perfusion and cardiac output, otherwise known as "the 5-in-1
maneuver" magic touch (Figure 5). ).
Figure 5. The “5-in-1 maneuver” magic touch–CCTV-R
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Source: Dengue clinical management: facilitator's
training manual. WHO 2013.
The patient is said to be in shock if the pulse pressure

(the difference between systolic and diastolic pressure) is
≤20 mmHg in children. Clinical signs of decreased capillary
perfusion (cold extremities, prolonged capillary refill time,
or rapid pulse). Hypotension is generally associated with
prolonged shock complicated by heavy bleeding. Severe
dengue should be suspected if someone living in an area at
risk for dengue infection presents with fever for 2–7 days
accompanied by the following symptoms:12
a. There is evidence of plasma leakage such as a rapidly

rising/high hematocrit and/or pleural effusion, ascites.
b. Shock with tachycardia, clammy and cold extremities,
capillary refill time of more than two seconds, weak or
absent pulse, narrow pulse pressure or, in advanced
shock, unmeasured blood pressure.
c. There is significant/massive/severe bleeding (such as
gastrointestinal bleeding in the form of hematemesis
melena, heavy menstruation, respiratory tract bleeding
in the form of hemoptysis, urinary tract bleeding in the
form of hematuria, extensive skin bleeding in the form
of purpura, ecchymosis or bruising at the injection
site).
d. There is a change in consciousness (lethargy or

restlessness, coma, seizures).
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e. There is severe gastrointestinal disturbances.
f. There is severe organ damage (acute liver failure,

acute renal failure, encephalopathy or encephalitis,
cardiomyopathy or other unusual manifestations).
Further explanation regarding the definition of shock

and organ involvement in dengue infection is as follows: 12
a. Shock:
1) Poor capillary perfusion is characterized by

increased pulse rate (tachycardia), capillary refill
time of more than two seconds, cold extremities.
2) Pulse pressure narrows (<20 mm Hg).
3) Hypotension or until immeasurable.
4) The pulse feels weak and small until it can't be felt.
b. Hypotension:
A decrease in systolic blood pressure >40 mm Hg or

<2 SD below normal for the age group.
c. Respiratory distress (shortness of breath):
1) Respiratory rate increases with age.
2) Increased work of breathing (dyspnea).
3) Kussmaul breath.
4) Saturation 02 ≤94% without administration 02.
5) Respiratory failure.
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d. Cardiac involvement in the form of:
1) myocarditis.
2) Cardiomyopathy.
3) Heart failure.
e. Involvement of the central nervous system, in the form of:
1) Decreased consciousness without finding

metabolic disturbances or other explanations, or
finding the following signs:
1) cerebrospinal fluid leukocytes >5/L; 2) focal
neurological signs, and 3) seizures (not simple
febrile seizures).
2) Encephalopathy.
3) Encephalitis.
f. Renal involvement, in the form of:
1) Serum creatinine ≥2x compared to the upper limit of normal

value.
2) Serum creatinine >1.2 mg/dL.
Assessment of AKI using the criteria of pediatric

RIFLE (RIFLE, an acronym for Risk of renal
dysfunction, Injury to the kidney, Failure of
kidney function, Loss of kidney function, and
End-stage Renal Disease
g. Liver involvement, in the form of:
1) Fail heart I which be marked with
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jaundice,thromboplastin time <20%, and
encephalopathy.
2) Enhancement function heart without
because other asHepatitis A, B, C,
or drug toxicity.
h. Severe bleeding (in the digestive tract) is:
1) Bleeding which need effort

blood/product transfusions.
2) Bleeding resulting in hemodynamic disturbances.
3) Bleeding that needs to be controlled by giving

nasal packing and dental splints.
2. PresumptiveDengue
If a person lives or travels to a dengue endemic area,

has a fever accompanied by the following two criteria: 12
a. Nauseous vomit.
b. Rash.
c. Pain and soreness.
d. Positive tourniquet test.
e. Leukopenia.
f. Warning signs.
3. Differences in Dengue Infection Classification
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The use of a new classification certainly requires an
adjustment in time and in order to facilitate its application,
Table 5 shows the equivalent of the new classification with
the classification that has been used. This is expected to
facilitate the use of the new classification.
Table 5. Classification of dengue infection diagnoses
1997 2011 New classification

Dengue fever Dengue Govern
(without fever Dengue anceGr
plasma (without without warning signs oup A
leakage) attenuation
Plasma
DHF degree I DHF degree I
(without shock) (without Govern
shock) anceGr
Dengue oup B
DHF grade II DHF degree
(without II with warning signs
EDS*
(without
shock, shock, but
however there is
bleeding
there is spontaneous)
spontaneous
bleeding)
DHF grade III DHF degree
(syndrome III Severedengue (seepage
(shock
dengue shock) syndrome plasmableeding, heavy Govern
22
dengue) bleeding, and organ
involvement) anceGr
DHF grade IV DHF IV oup C
(syndrome degree
dengue (dengue
shock shock
syndrome
withprofound with profound
shock) shock)
*EDS: Expanded dengue syndrome (unusual manifestations,
organ involvement, comorbidities)
3.1.6 Enforcement of Diagnosis
1.Dengue Diagnostic Test
Various laboratory diagnostic methods have

been developed to support patient management and
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disease control. The choice of diagnostic method
depends on the purpose of the test being performed
(eg clinical diagnosis, epidemiological survey,
vaccine development), the type of laboratory facility
and technical expertise available, cost, and when
sampling will be taken (Figure 6). Rapid test
examination can be done through serum, plasma or
blood to detect NS-1 virus antigen in the febrile
phase and IgM and IgG antibodies either in the
critical or convalescent phase. Virus examination in
the form of culture and molecular PCR can be done if
the facilities and infrastructure are available. The
chart below shows the best time to do a dengue
diagnostic test.
Figure 6. Diagnostic test options for dengue infection

control, 2009. with modification
2. Weir test (tourniquet test)
The weir test, also known as the Rumpel-Leede

test for dengue infection, has a sensitivity of 58% (95%
CI 43%-71%) and a specificity of 71% (95% CI 60%-
80%), whereas in dengue without a warning sign the
sensitivity is 55 % (95%CI 52%-59%) and specificity
63% (95%CI 60%-66%), in dengue with a warning
sign sensitivity 62% (95%CI 53%-71%) and specificity
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60% (95 %CI 48%-70%) with an AUC accuracy of
0.70 (95% CI 0.66-0.74). In children it is necessary to
use the appropriate cuff. A positive weir test increases
the chance of dengue infection.
3. Hematocrit and Complete Peripheral Blood
Monitoring of hematocrit (Ht) and complete

peripheral blood (DPL), is required as follows:
a. Hematocrit (not hemoglobin) is one of the tests to

determine the occurrence of hemoconcentration or
increased capillary permeability (plasma seepage).
The hematocrit shows the evolution of the disease
and the response to fluid therapy.
b. Ht examination is carried out at the first visit of
dengue patients (in the febrile phase or before
entering the critical phase).
c. An increase in hematocrit followed by a rapid
decrease in platelet count (≤100,000/mm3) is one
of the warning signs.
d. An increased hematocrit that does not decrease
with fluid therapy is a sign of severe plasma
leakage, whereas in severe dengue a decreased
hematocrit can be a sign of bleeding.
e. Leukopenia is often found in dengue with
leukocyte counts even reaching <2000/mm3.
f. In dengue infection the total number of leukocytes,
neutrophils and platelets is lower when compared
to patients with fever caused by other viruses in
dengue endemic areas. (Recommendation A, level
of evidence rating I)
g. Other Laboratory Tests and Imaging
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The table below shows the laboratory and imaging
tests performed on severe dengue patients. Examination is
carried out according to indications and if the patient has
comorbidities (additional diseases).
Table 6. Other investigations for dengue infection
Supporting investigation Indication

Blood chemistry:
- liver and kidney function - Severe plasma leakage and organ damage
- cardiac enzymes severe dengue
- blood sugar, albumin, lactate - myocarditis
- Shock in severe dengue
Blood gas analysis Shock
Electrolyte Severe plasma leakage and organ disturban
on severe Dengue
coagulation factor Bleeding and/or disturbances
Coagulation
Urine Renal impairment and bleeding
Stool Gastrointestinal bleeding
Hemodynamic monitoring tool Shock hypotensive and/or refractory
- non-invasive
- invasive
Electrocardiogram myocarditis
Electrolyte disturbances
Echocardiography Heart problems

Chest x-ray examination: detect effusion pleura
- right lateral decubitus ondengue infection
- PA/AP detect abnormality lungsincludi
pulmonary edema and post
installation of devices
Abdominal and thoracic ultrasound detect ascites, pleural effusion, organomega
and gallbladder wall thickening. Also
determine the adequacy of the liquid
measuring the collapsibility index
IVC
CT-scanhead without contrast detect bleedingintracranial
encephalopathy if dengue is accompanied
neurological symptoms, such as seizures and
loss of consciousness
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3.1.7 Governance
The management of dengue infection is

relatively simple, inexpensive, and very effective in
saving the patient's life as long as the intervention is
carried out correctly and in a timely manner. The key
lies in early identification, precisely determining sick
days so that you can place them in the phases of the
disease, and understanding the clinical problems that
occur in each phase.
Triage activities in outpatient/polyclinic,

emergency room, or inpatient care must pay attention
to the following:
ii. Recognize fever as a sign and symptom of dengue.
iii. Manage dengue patients from the beginning of the

febrile phase and monitor patients without warning
signs every day.
iv. Recognize the early stages of plasma leakage or the
critical phase of dengue and initiate fluid therapy.
v. Recognize patients with warning signs requiring
treatment and/or administration of intravenous fluids.
vi. Referring patients to health care facilities that are more
complete/higher.
vii. Recognize and manage patients with severe dengue
(severe plasma leakage, shock, severe bleeding and
severe organ damage) promptly and appropriately.
viii. Early notification of patients with dengue to the local
27
Health Office.
Based on history, physical examination and/or

peripheral blood examination
complete and hematocrit, as well as confirmation of

dengue if possible, the doctor must be able to
determine whether the infection is caused by dengue,
what phase is it (febrile, critical or recovery phase),
whether there are warning signs, what is the hydration
status and hemodynamic status of the patient, and
whether the patient should be treated (Table 8) or
discharged (Table 9).
Table 8. Criteria for hospitalization
Warning signs Every warning sign (see Table 3)

Signs and symptoms associated The patient is dehydrated, unable to take oral fluids
with hypotension (possibility of Dizziness or postural hypotension
plasma leakage) Profuse sweating, decreased consciousness,
worsening condition during defervescence
Hypotension or cold extremities
28
Bleeding Bleeding spontaneous, no depends
total
Platelets
Organ damage Kidney, liver, nerves, or heart
- enlarged liver, pain, although not yet shocked
- chest pain or respiratory distress, cyanosis
Findings through Hematocrit increases
inspectionFurthermore Pleural effusion, ascites, asymptomatic gallbladder
thickening
Warning signs Every warning sign (see Table 3)

Accompanying conditions Comorbid conditions such as congenital heart
disease, thalassemia, diabetes mellitus, gastric ulcers,
and others
Overweight or obesity (immediate intravenous
access in the emergency room)
Baby
Social problem Living alone/boarding
Live far from health facilities. Without
adequate transportation

control, 2009.
29
Table 9. Criteria for patients who can be discharged
Clinical No fever for 48 hours

Improved clinical status (general health, appetite, hemodynamic
condition, urine output, no respiratory distress, no signs of
myocarditis)
Laboratory Platelet count tends to increase >50,000/uL
Stable hematocrit without administration of intravenous fluids

control, 2009.
Treatment decisions depend on clinical manifestations and

other circumstances (Figure 6), patients may be discharged
(Group A), referred for in-hospital treatment (Group B), or
require emergency treatment and immediate referral (Group
C). It should be noted, the clinical manifestations of dengue
can change and are difficult to predict, however, the
management given is consistent according to the patient's
condition at the time of examination (present status).
30
Figure 6. Diagram/Flow of Management of Dengue Infection
Source: WHO. Dengue guidelines for diagnosis,
treatment and control, 2009.
1. Management of Groups A, B, and C
a. Group A – Outpatient
31
Patients who were discharged home for outpatient
management.
Patients in group A are those who are still able to drink

sufficient amounts and urinate at least once every 6 hours
and do not have warning signs (Figure 7), especially when
the fever goes down (defervescense).
Figure 7. Management of Group A outpatients

treatment and control, 2009
Outpatients must control the polyclinic every day to

monitor their clinical progress (drinking intake,
diuresis, and activity) until they pass the critical phase.
Patients with stable hematocrit levels can be
discharged home by following the following home
care recommendations12:
1) Remind them to immediately take the patient to

the hospital if warning signs are found.
2) Increase fluid intake by giving oral rehydration
solutions (ORS), fruit juices, and other fluids
containing electrolytes and sugars to replace
32
fluids lost by fever and vomiting.
3) Give paracetamol for high fever at intervals 4–6

hours. Give warm compresses if the patient still
has a high fever. Do not give acetylsalicylic acid
(aspirin), ibuprofen, or non-steroidal anti-
inflammatory drugs (NSAIDs) because these
drugs can cause gastritis or bleeding. Acetyl
salicylic acid may be associated with the
occurrence of Reye's syndrome.
Table 10. Instructions for treating dengue patients at home

Instructions for treating dengue patients at home
What to do?
- Adequate bed rest
- Adequate fluid intake (>5 glasses for adolescents)
 Milk, fruit juice and isotonic electrolyte fluids (ORS) and rice or
barley water
 Plain/fresh water alone can cause an electrolyte imbalance
- Give oral paracetamol (no more than 75 mg/kg/day with a maximum dose of
4 g/day)
- Compress and wipe with warm water
- Check and eradicate mosquito nests in or around the house
What to avoid?
- Do not take drugs that contain acetylsalicylic acid (aspirin), mefenamic acid
(ponstan), ibuprofen, or other non-steroidal anti-inflammatory drugs
(NSAIDs), or steroids. Consult a doctor if the patient has taken this drug
before.
- Antibiotics are not needed.
If the following symptoms are found, take the patient to the nearest hospital.
These symptoms are warning signs for hazardous conditions:
1) Bleeding:
o Red patches of skin in various places
o Nosebleeds or bleeding gums that are difficult to stop
o Vomiting blood
o Black stools
o Heavy menstruation that is more than usual
2) Frequent vomiting
3) Severe abdominal pain
4) Frequent drowsiness, mental confusion or seizures
5) Hands and feet damp, cold and pale
6) Difficulty breathing
33
Source: WHO. Dengue guidelines for
diagnosis, treatment and control, 2009. with
modification
Outpatients must be monitored daily by health

workers to find out patterns of temperature, fluid intake and
output, diuresis (amount of urine released), warning signs,
signs of plasma seepage and bleeding.
hematocrit, leukocyte and platelet counts. Patients are given

a home care card as listed in Table 10.
b. Group B – Patients who must be referred for hospital

treatment
Patients need to be referred to secondary health
care facilities (hospitals) for more stringent monitoring
especially when entering a critical phase. During inpatient
monitoring of dengue patients at the hospital, 52 (28%) out
of 185 dengue fever could develop into dengue shock
syndrome (severe dengue), so monitoring of vital signs,
warning signs, and hematological examinations needs to be
done periodically. Group B treatment is for patients with
warning signs or with comorbidities (risk factors) that will
make management more complex, for example infants,
obesity, comorbidities (diabetes mellitus, hemolytic
disease, kidney failure), or if special social conditions are
found. for example living far from health facilities with
limited access to transportation,
34
Figure 8. Group B: Dengue with accompanying conditions, but without warning signs
and control, 2009.
If the patient does not find warning signs, the

action plan that must be carried out is as follows. Instruct
patient to drink more. If these are not met, start
intravenous fluid therapy with 0.9% NaCl (normal saline)
or Ringer's lactate with or without dextrose by
maintenance drip (Figure 9). For patients who are obese or
overweight, use ideal body weight to calculate the amount
of fluid administered (Table 11 and Table 12). Give
sufficient intravenous fluids to maintain good perfusion
and adequate diuresis
Table 11. Number of fluid administration per hour for

patients with excess body weight
35
Fluid normal Administration of Fluid
maintenance fluids based on 2-3 administratio
(ml/hour) ml/kg/hour n based on
based onHolliday (ml/hour) 1.5-2
formula - Fresh ml/kg/hour
(ml/hour)
10 10-15
10 20 20-30
15 30 30-45
20 60 40-60
25 65 50-75
30 70 60-90
35 75 70-105
40 80 80-120
50 90 100-150
60 100 90-120
70 110 105-140
80 120 120-150
Notes:
For IBW >50 kg, 1.5-2 ml/kg is used for rapid

calculation of hourly maintenance fluid
administration. For IBW ≤50 kg, 2- 3 ml/kg is used for
quick calculation of maintenance fluid administration
per hour
Table 12. Estimated ideal body weight (IBW) for

overweight and obesity
36
Height(cm) Estimated male IBW (kg). Estimated female IBW
(kg).
150 50 45.5
160 57 52
170 66 61.5
180 75 70
treatment and control, 2009
Patients should be monitored for temperature

patterns, volume of fluid in and out, amount of urine
(volume and frequency), warning signs, hematocrit
levels, leukocyte and platelet counts (Table 13). Other
laboratory tests (such as liver, kidney, heart and
hemostasis functions) can be performed, depending on
the clinical picture and the facilities available at health
services.
If the patient has warning signs, the action

plan that must be carried out includes the following
1) Check the hematocrit before giving fluid

therapy. Give isotonic solutions such as 0.9%
NaCl (normal saline), Ringer's lactate, or
Hartmann's solution. Start with 5–7 ml/kg/hour
drip for 1–2 hours according to clinical and/or
laboratory indications (eg dehydration, plasma
leakage), then reduce to 3–5 ml/kg/hour for 2–4
hours, and reduced to 2–3 ml/kg/hour or less
based on clinical response
2) Recheck the clinical condition and repeat the
hematocrit. If the hematocrit remains the same
or increases only slightly, continue to give the
same fluids (2–3 ml/kg/hour for the next 2–4
37
hours). If vital signs worsen and the hematocrit
is increasing rapidly, increase the volume to 5–
10 ml/kg/hour for the next 1–2 hours.Reassess
clinical condition, re-check hematocrit and
determine the number of drops of fluid
according to condition.
3) Give sufficient intravenous fluids to maintain

good tissue perfusion and maintain a diuresis of
1 ml/kg/hour. Intravenous fluids are generally
given only over 24–48 hours. Reduce
intravenous fluids gradually as the rate of plasma
leakage decreases. This can be seen from the
amount of urine output and/or oral fluid intake
that improves, or a decrease in the hematocrit
below the baseline value with a stable patient
condition
4) Patients with warning signs must be monitored
by health workers (doctors and/or nurses) until
the critical phase has passed. Fluid balance must
be maintained. Parameters to be monitored
include vital signs and peripheral perfusion
(every 1–4 hours until the critical phase is
passed), urine output (every 4–6 hours),
hematocrit (before and after fluid administration,
then every 6–12 hours thereafter), glucose blood,
and other organ functions (such as kidney
function, liver function, coagulation, checked as
indicated).
38
Figure 9. Group B: Dengue with warning signs (no
shock): inpatient fluid management
and control, 2009. with modification
39
Figure 10. Group B: Dengue with warning signs (no
shock): no improvement after the first fluid
administration
and control, 2009.
c. Group C – Patients requiring immediate referral and

emergency treatment (severe dengue)
Patients need emergency care and immediate
referral if the following conditions are encountered in the
critical phase:
1) Intense plasma leakage causing shock and/or

fluid accumulation with respiratory distress.
2) Heavy bleeding.
3) Severe organ damage (liver failure, impaired

renal function, cardiomyopathy, encephalopathy
or encephalitis).
Patients with severe dengue require

hospitalization in hospitals that have intensive care
facilities and blood transfusion units. Adequate and
timely administration of intravenous fluids is
essential and is the only therapy needed. Isotonic
crystalloid solutions are optional and must be given
in sufficient quantities to maintain good tissue
circulation during the plasma leakage phase. 11
Fluid administration should be continued to

replace lost plasma and maintain good circulation
over the next 24–48 hours. For patients who are
overweight or obese, ideal body weight is used to
calculate the number of fluid drops administered
(Tables 8 and 9). Blood typing and cross matched
testing should be performed for all patients in shock.
40
Blood transfusions are only given for cases with
suspected heavy bleeding, for example in
gastrointestinal bleeding
Fluid resuscitation is a step of giving

intravenous fluids in large quantities (eg 10–20
ml/kg/bolus) in a short time with close supervision to
determine the response to the procedure and prevent
the possibility of pulmonary edema due to fluid
overload. The degree of intravascular volume deficit in
dengue shock varies. Fluid intake (input) is generally
greater than output (output), however, calculating the
input/output ratio is not important to assess fluid needs
in this phase.
The goal of fluid resuscitation is to improve

central and peripheral blood circulation (pulse rate
drops/tachycardia decreases, blood pressure improves,
pulse volume increases, extremities are warm, and
capillary refill time is <2 seconds) and increases organ
(end-organ) perfusion – examples : stable
consciousness (more patient/restless/less fussy),
diuresis ≥1 ml/KgBB/hour, improved metabolic
acidosis.
2. Management of Shock
Initial management of emergencies in shock

conditions includes assessment and management of
airway, breathing and circulation12.
a. airways(airway)
Assessment of airway patency in children with shock

is carried out using the 'look, listen, feel' technique, which is
to open the airway in a sniffing position, then watch for
chest development while listening to breath sounds and
41
feeling the air coming out of the nose/mouth. The results of
airway assessment are classified as follows:
2. Free airway: when spontaneous breathing seems adequate.

3. The airway can still be maintained with simple tools such as
oropharyngeal airwayor a nasopharyngeal airway.
4. The airway must be maintained by intubation if the patient is
apneic or gasping.
b.Breathing(breathing effort)
Assessing respiratory effort begins by counting the

number of breaths. Assessment of respiratory frequency
was carried out for 1 minute and the results were plotted
in the table of normal respiratory frequency values for
children according to age. The results of the assessment of
respiratory frequency are classified as follows:
 Tachypnea.
 Bradypnea.
 apnea
Assessment of respiratory effort is done by seeing,

hearing, also using a stethoscope and pulse-oxymetry
device if available. A reading above 94% saturation can
roughly indicate adequate oxygenation. A reading below
90% in a child on 100% oxygen may indicate that the child
needs a ventilator. Interpretation of pulse oximetry should
be carried out together with effort assessment breath,
respiratory rate and appearance of the child. Children with
42
respiratory problems are sometimes still able to maintain
blood oxygen levels bywork of breathingwhich increases.
In the initial management of shock, give oxygen with 100%
FiO2 using a mask with a reservoir. If the patient's
condition is stable the FiO2 can be titrated down until the
oxygen saturation is in the range of 94-98%.
C.circulation(circulation)
Immediately install peripheral intravenous access or

intraosseous if within 90 seconds the installation of
peripheral intravenous access fails. Insert a urinary catheter
to monitor diuresis and optimal fluid balance.
43
Figure 11. Group C: Emergency management of compensated
shock (maintained systolic pressure + reduced peripheral
perfusion)
control, 2009. with modification
Action plans performed in patients with

compensated shock (Table 4, Figures 10, 11 and 13).
 oxygenation.
 Initiate intravenous fluid resuscitation with isotonic
crystalloid solution in 10–20 drops
ml/kg/hour for one hour. (Recommendation A, level
I evidence rating), then
Reassess the patient's general condition (vital signs, capillary
refill time,
hematocrit, urine output).
 If the patient's clinical condition improves,

intravenous fluids should be reduced gradually
to 5–7 ml/kg/hour for 1–2 hours, then 3–5
ml/kg/hour for 2–4 hours, decreasing to 2–3
ml/kg. /hour and thereafter depending on the
hemodynamic conditions maintained for 24–48
hours (Tables 8 and 9).
 If the vital signs are still unstable (the patient is
still in shock), check the hematocrit after the
first bolus. If the hematocrit is still high
(>50%), repeat a second bolus of 10–20
ml/kg/hour of crystalloid solution within one
hour. After the second bolus, if there is
improvement, reduce the number of drops to
7–10 ml/kg/hr for 1–2 hours, then continue to
44
reduce the drip as above. If the hematocrit is
lower than the initial hematocrit value, eg:
<40% for girls, <45% for boys; well-
nourished), and this unstable condition
suggests bleeding, a cross-matched test and
blood transfusion are needed as soon as
possible (as appropriate treatment for bleeding
complications).
 Crystalloid fluid or colloid boluses may still be
needed in the next 24 hours (depending on
conditions). The number and rate of infusion
drops are adjusted according to clinical
response.
 Initial hematocrit examination will assist in
assessing the success of fluid therapy and
efforts are made to carry out investigations to
assess organ function.
45
3.2 Mild Moderate Dehydration Acute Diarrhea
3.2.1 Definition
Acute diarrhea is defecation in infants or children more than 3 times per day,
accompanied by a change in the consistency of the stool to liquid with or without mucus
and blood that lasts less than one week. In babies who drink breast milk, the frequency of
defecation is more than 3-4 times per day, this condition cannot be called diarrhea, but it is
still physiological or normal. As long as the baby's weight increases normally, this is not
classified as diarrhea, but is a temporary lactose intolerance due to incomplete
development of the digestive tract. For babies who drink exclusively breast milk, the
practical definition of diarrhea is an increase in the frequency of bowel movements or the
consistency becomes liquid, which according to the mother is abnormal or not as usual.
Sometimes a child defecates less than 3 times per day,
3.2.2 Etiology
At present, with advances in laboratory techniques, pathogenic germs can be

identified from diarrhea sufferers, around 80% of cases that come to health facilities and
around 50% of mild cases in the community. At this time no less than 25 types of
microorganisms can be identified that can cause diarrhea in children and infants. The main
infectious causes of diarrhea are generally viruses, bacteria and parasites. The two basic
types of acute infectious diarrhea are non-inflammatory and inflammatory. 1,2,8
Enteropathogens cause non-inflammatory diarrhea through production of enterotoxins by
bacteria, destruction of villi surface cells by viruses, attachment by parasites, attachment
and/or translocation of bacteria. In contrast, inflammatory diarrhea is usually caused by
bacteria that invade the gut directly or produce cytotoxins. Some of the causes of acute
diarrhea that can cause diarrhea in humans are as follows13:
Bacterial Group:
1. Aeromonas
2. Bacillus cereus
3. Campylobacter jejuni
4. Clostridium perfringens
5. Clostridium defficile
6. Escherichia coli
7. Plesiomonas shigeloides
8. Salmonella
9. Shigella
10. Staphylococcus aureus
11. Vibrio cholera
12. Vibrio parahaemolyticus
13. Yersinia
Viruses:
1. Astrovirus
2. Rotavirus
3. Calcivirus (Norovirus, Sapovirus)
4. Norwalk virus
5. Enteric adenovirus
6. Herpes simplex virus
7. Coronaviruses
8. Cytomegalovirus *
Parasites:
1. Balantidium coli
2. Giardia lamblia
3. Blastocystis homonis
4. Isospora belli
5. Cryptosporidium parvum
6. Strongyloides stercoralis
7. Entamoeba histolytica
8. Trichuris trichiura
3.2.3 Mechanism of Diarrhea

In general, diarrhea is caused by 2 things, namely interference with the process of
absorption or secretion. There are several divisions of diarrhea14:
1. Distribution of diarrhea according to etiology

2. The distribution of diarrhea according to the mechanism, namely interference a.
absorption b. Secretory disorders.
3. Distribution of diarrhea according to duration of diarrhea: Acute diarrhea lasting less
than 14 days. Chronic diarrhea lasting more than 14 days with non-infectious etiology.
Persistent diarrhea lasting more than 14 days with infectious etiology.
The occurrence of diarrhea in general occurs from one or several overlapping

mechanisms. According to the mechanism of diarrhea, it is known: Diarrhea due to
absorption disorders, namely the volume of fluid in the colon is greater than the absorption
capacity. Here diarrhea can occur due to abnormalities in the small intestine, resulting in
decreased absorption or increased secretion. If the function of the small intestine is normal,
diarrhea can occur due to decreased absorption in the colon or increased secretion in the
colon. Diarrhea can also be associated with motility, inflammation and immunological
disorders.
1. Impaired absorption or osmotic diarrhea.

In general, there is a decrease in absorption function for various reasons such as celiac
sprue, or because:
a. take magnesium hydroxide
b. sucrase-isomaltase deficiency presence of lactase deficiency in older children
c. The presence of material that is not absorbed causes the intraluminal material
in the proximal small intestine to become hypertonic and cause
hyperosmolarity. As a result of the difference in osmotic pressure between the
intestinal lumen and the blood, in the permeable segment of the jejunum, water
will flow towards the jejunum lumen, so that a lot of water will accumulate in
the intestinal lumen. Na will follow into the lumen, thus a large amount of
intraluminal fluid will collect with normal Na levels. A small portion of this
fluid will be reabsorbed, but others will remain in the lumen because there are
materials that cannot be absorbed such as Mg, glucose, sucrose, lactose,
maltose in the ileum segment and exceed the absorption capacity of the colon,
resulting in diarrhea. Ingredients such as carbohydrates from fruit juices,
2. General malabsorption.
Conditions such as short bowel syndrome, celiac, proteins, peptides, starches,

amino acids and monosaccharides have a role in osmotic movement in the intestinal
lumen. Damage to cells (which normally absorb Na and water) can be caused by
viruses or germs, such as Salmonella, Shigella or Campylobacter. These cells can also
be damaged by idiopathic inflammatory bowel disease, due to toxins or certain drugs.
A characteristic feature of the disease causing small intestinal malabsorption is villous
atrophy. Furthermore, certain microorganisms (overgrown bacteria, giardiasis, and
enteroadherent E. coli) cause malabsorption of nutrients by changing the function of
the brush border membrane without damaging the anatomical arrangement of the
mucosa. Maldigestion of complete proteins, carbohydrates,
Disturbance or failure of pancreatic excretion causes failure to break down

complex proteins, carbohydrates, triglycerides, then causes maldigestion,
malabsorption and finally causes osmotic diarrhea. Steatorrhe differs from protein and
carbohydrate malabsorption with intraluminal long-chain fatty acids, not only causing
osmotic diarrhea, but also causing racing of Cl- secretion so that diarrhea can be
caused by carbohydrate malabsorption due to diffuse damage to the intestinal mucosa,
sucrose deficiency, isomaltose and congenital lactase deficiency. administering
laxatives; lactulose, administration of Mg hydroxide (eg milk Mg), excessive
carbohydrate malabsorption in hypermotility in irritable colon. Get hypertonic fluids in
large quantities and quickly, causing recurrence of diarrhea. Feeding/drinking high
KH, after experiencing diarrhea, causing a recurrence of diarrhea. Viral infections that
cause mucosal damage resulting in impaired secretion of the lactase enzyme, resulting
in impaired absorption of lactose nutrients
3. Impaired secretion or secretory diarrhea. Hyperplasia of the crypts.
Theoretically, crypt hyperplasia due to any disease, can cause intestinal

secretions and diarrhea. In general, this disease causes villous atrophy. Luminal
secretagogues are known to have 2 ingredients that stimulate lumen secretion, namely
bacterial enterotoxins and chemicals that can stimulate such as laxants, dihydroxy
form of bile salts, and long chain fatty acids. This toxin that causes diarrhea primarily
works by increasing the intracellular concentration of cAMP, cGMP or Ca++ which in
turn activates protein kinases. Activation of protein kinases will cause phosphorylation
of protein membranes resulting in changes in ion channels, will cause Cl- in the crypt
to come out. On the other hand, there is an increase in the sodium pump, and sodium
enters the intestinal lumen with Cl-. Laxatives can cause a variety of effects on NaK-
ATPase activity. Some of them stimulate an increase in intracellular cAMP levels,
increase intestinal permeability and some cause damage to mucosal cells. Some drugs
cause intestinal secretions. Malabsorption diseases such as ileal resection and Crohn's
disease can cause secretory abnormalities such as causing increased concentrations of
bile salts, fats.
Blood-Borne Secretagogues. Secretory diarrhea in children in developing

countries, generally caused by E coli or cholera enterotoxins. In contrast to developing
countries, in developed countries, secretory diarrhea is rarely found, if there is a
possibility that it is caused by drugs or tumors such as ganglioneuroma or
neuroblastoma that produce hormones such as VIP. In adults, severe secretory diarrhea
is caused by pancreatic neoplasms, non-beta cells that produce VIP, pancreatic
polypeptide, other secretory hormones (watery diarrhea hypokalemia achlorhydria
(WDHA) syndrome). Diarrhea caused by this tumor is rare. 5 All disorders of the
intestinal mucosa result in excessive water and mineral secretion in the villus and
crypts and all enterocytes are involved and can occur in the intestinal mucosa under
normal circumstances.
4. Diarrhea due to peristaltic disorders
Although motility is rarely the primary cause of malabsorption, changes in

motility do have an effect on absorption. Either increased or decreased motility, both
can cause diarrhea. Decreased motility can cause bacteria to overgrow which causes
diarrhea. Slowing transit of drugs or nutrients will increase absorption. Severe
intestinal motility failure causes intestinal stasis resulting in inflammation, bile salt
deconjugation and malabsorption. Diarrhea due to hyperperistalsis in children is rare.
Watery diarrhea can be caused by hypermotility in cases of irritable colon in infants.
Motility disorders may be a cause of diarrhea in thyrotoxicosis, malabsorption of bile
acids and various other diseases
5. Inflammatory diarrhea
Inflammatory processes in the small intestine and colon cause diarrhea in a

number of circumstances. Due to loss of epithelial cells and damage to tight junctions,
hydrostatic pressure in the blood and lymphatic vessels causes water, electrolytes,
mucus, protein and often red and white blood cells to accumulate in the lumen.
Usually this inflammatory diarrhea is associated with other types of diarrhea such as
osmotic diarrhea and secretory diarrhea. Pathogenic enteral bacteria will affect the
structure and function of the tight junction, induce fluid and electrolyte secretion, and
will activate the inflammatory cascade. The effect of bacterial infection on tight
junctions will affect the anatomical arrangement and function of absorption, namely
the cytoskeleton and changes in protein composition. Research by Berkes J et al. 2003
showed that the role of pathogenic enteral bacteria in diarrhea lies in changing the tight
junction barrier by toxins or germ products, namely changes in the cellular
cytoskeleton and specific tight junctions. The influence can be on both components or
just one component so that it will cause chloride hypersecretion which will be
followed by sodium and water. For example, C. difficile will induce cytoskeleton and
protein damage, Bacteroides fragilis causes proteolytic degradation of tight junction
proteins, V cholera affects the distribution of tight junction proteins, while EPEC
causes accumulation of cytoskeleton proteins. The influence can be on both
components or just one component so that it will cause chloride hypersecretion which
will be followed by sodium and water. For example, C. difficile will induce
cytoskeleton and protein damage, Bacteroides fragilis causes proteolytic degradation
of tight junction proteins, V cholera affects the distribution of tight junction proteins,
while EPEC causes accumulation of cytoskeleton proteins. The influence can be on
both components or just one component so that it will cause chloride hypersecretion
which will be followed by sodium and water. For example, C. difficile will induce
cytoskeleton and protein damage, Bacteroides fragilis causes proteolytic degradation
of tight junction proteins, V cholera affects the distribution of tight junction proteins,
while EPEC causes accumulation of cytoskeleton proteins.
6. Immunologically related diarrhea

Immunologically associated diarrhea is associated with type I, III and IV
hypersensitivity reactions. Type I reactions are reactions between mast cells and IgE
and food allergens. Type III reactions are for example in gastroenteropathy, while type
IV reactions are found in Celiac disease and protein loss enteropathies. In type I
reactions, allergens that enter the body cause an immune response with the formation
of IgE which will then be bound by specific receptors on the surface of mast cells and
basophils. If there is activation due to repeated exposure to specific antigens, mast
cells will release mediators such as histamine, ECF-A, PAF, SRA-A and
prostaglandins. In type III reactions, antigen-antibody complex reactions occur in
tissues or blood vessels that activate complement.
3.2.4 Clinical Manifestations
Clinical Manifestations Intestinal infections cause gastrointestinal signs and

symptoms and other symptoms if there are extra-intestinal complications including
neurologic manifestations. Gastrointestinal symptoms can include diarrhea,
stomach cramps and vomiting. While systemic manifestations vary depending on
the cause. Sufferers with watery diarrhea excrete feces that contain large amounts
of sodium, chloride and bicarbonate ions. This loss of water and electrolytes
increases when there is vomiting and water loss also increases when there is heat.
This can lead to dehydration, metabolic acidosis and hypokalemia. Dehydration is
the most dangerous condition because it can cause hypovolemia, cardiovascular
collapse and death if not treated properly. Dehydration that occurs according to
plasma tonicity can be isotonic dehydration,
According to the degree of dehydration can be without dehydration, mild

dehydration, moderate dehydration or severe dehydration. Extraintestinal infections
associated with pathogenic enteric bacteria include: vulvovaginitis, urinary tract
infections, endocarditis, osteomyelitis, meningitis, pneumonia, hepatitis, peritonitis
and septic thrombophlebitis. Neurologic symptoms of intestinal infection may
include paresthesia (due to eating fish, shellfish, monosodium glutamate) hypotonia
and muscle weakness (C. botulinum).
3.2.5 Diagnosis
3.2.5.1 Anamnesis
In the anamnesis it is necessary to ask the following: duration of diarrhea,
frequency, volume, stool consistency, color, odor, presence/absence of mucus and
blood. If accompanied by vomiting: volume and frequency. Urinary: regular,
reduced, infrequent or not urinating in the last 6-8 hours. Food and drink given
during diarrhea. Is there fever or other accompanying diseases such as: cough,
runny nose, otitis media, measles. Actions taken by the mother while the child has
diarrhea: giving ORS, bringing treatment to the health center or hospital and the
medicines given and the immunization history.
3.2.5.2 Physical examination

On physical examination it is necessary to check: body weight, body
temperature, heart and respiratory rate and blood pressure. Furthermore, it is
necessary to look for the main signs of dehydration: consciousness, thirst and
abdominal skin turgor and other additional signs: sunken fontanel or not, eyes:
male or not, presence or absence of tears, lips, oral mucosa and dry or wet tongue.
Rapid breathing and indicative of metabolic acidosis. Weak or absent bowel sounds
when hypokalemia is present. Examination of the extremities is necessary because
perfusion and capillary refill can determine the degree of dehydration that occurs.
Assessment of the severity or degree of dehydration can be determined in an
objective way, namely by comparing the body weight before and during diarrhea.
Subjectively using WHO criteria, Maurice King Score,
Table 13. Determination of the degree of dehydration according to WHO 1995
Table 14. Determination of the degree of dehydration according to the numerical system – Maurice
King (1974)
The results obtained in patients are given a number of 0, 1 or 2 according to the table and then
added up. Score: 0 – 2 = Mild 3 – 6 = Moderate 7 – 12 = Severe
3.2.5.3 Laboratory
Complete laboratory examination in acute diarrhea is generally not needed, only in

certain circumstances it may be needed, for example the underlying cause is unknown or
there are other causes besides acute diarrhea or in patients with severe dehydration.
Example: complete blood count, urine and stool culture in sepsis or urinary tract infection.
Laboratory tests that are sometimes needed in acute diarrhea16,17:
- Blood: complete blood count, serum electrolytes, blood gas analysis, blood glucose,
culture and sensitivity test to antibiotics.
- Urine: complete urine, culture and sensitivity test to antibiotics.
- Feces :
- Macroscopic examination: Macroscopic examination of feces needs to be done in
all patients with diarrhea even though laboratory tests are not carried out. Stools
that are watery and without mucus or blood are usually caused by viral
enterotoxins, protozoa or caused by infections outside the gastrointestinal tract.
Stools that contain blood or mucus can be caused by bacterial infections that
produce cytotoxins, enteroinvasive bacteria that cause inflammation of the mucosa
or intestinal parasites such as: E. histolytica, B. coli and T. trichiura. If there is
blood, it is usually mixed in the stool except in infections with E. histolytica, blood
is often present on the surface of the stool, and in EHEC infection there are streaks
of blood in the stool. Foul-smelling stools are seen in infections with Salmonella,
Giardia, Cryptosporidium and Strongyloides.
- Microscopic examination: Microscopic examination to look for leukocytes can
provide information about the cause of diarrhea, anatomical location and the
presence of mucosal inflammatory processes. Leukocytes in the stool are produced
in response to bacteria that attack the colonic mucosa. Positive leukocytes on stool
examination indicate the presence of invasive germs or bacteria that produce
cytotoxins such as Shigella, Salmonella, C. jejuni, EIEC, C. difficile, Y.
enterocolitica, V. parahaemolyticus and possibly Aeromonas or P. shigelloides.
Leukocytes found in general are PMN leukocytes, except in S. typhii mononuclear
leukocytes. Not all colitis sufferers have leukocytes in their stools, patients infected
with E. histolytica generally have minimal leukocytes in their stools.
Normally no examination for eggs or parasites is required unless there is a
history of recent travel to a high-risk area, stool cultures are negative for
enteropathogens, diarrhea for more than 1 week or in an immunocompromised
patient. Patients suspected of having diarrhea caused by giardiasis,
cryptosporidiosis, isosporiasis and strongyloidiasis in which stool examination is
negative, upper duodenal or jejunal aspiration or biopsy may be required. Because
the organism lives in the upper digestive tract, this procedure is more precise than
examining a stool specimen. Duodenal biopsy is a specific and sensitive method for
the diagnosis of giardiasis, strongylodiasis and spore-forming protozoa. E.
hystolitica can be diagnosed by microscopic examination of fresh stools.Classiffdo
it signsThis is in accordance with the degree of dehydration table below
Mild/
Symptoms Severe dehydrating
Diarrhea moderate
/degree of diarrhea
without dehydrati
dehydratio
dehydratio on
n
n diarrhea
If there are If there are If there are two or more
two or more two or more signs
signs signs
general state Lethargic, limp /
Fine, sober Nervous,fussy
unconscious
Eye Not concave Sunken Sunken
Desire to Want to keep
Normal, no
drink drinking Lazy to drink
thirst
there is thirst
Come Back Returnvery slow
Turgor
back slow
soon
1. Diarrhea without dehydration: if there are two or more signs:
 General condition is good

 The eyes are not cowang
 Drink normally, not thirsty
 Abdominal skin pinch/turgor Return immediately.
Treatment Plan A (For treatment of diarrhea without dehydration)
Explain the 5 steps of treating diarrhea at home
1.Give more fluids than usual

- Continue to breastfeed more frequently and for longer
- Children who are exclusively breastfed, give ORS or boiled water in
addition
- Children who are not exclusively breastfed, give milk they usually drink
and ORS or household fluids in addition (vegetable broth, starch water,
boiled water, etc.)
- Give ORS until the diarrhea stops. If vomiting, wait 10 minutes and
continue little by little.
- Age < 1 year given 50-100 ml every time they defecate
- Age > 1 year given 100-200 ml every time they defecate.
• Children should be given 6 packets of ORS (200 ml) at home if:
- Have been treated on a Treatment Plan B or C.
- Cannot return to health workers if diarrhea worsens.
• Teach the mother how to mix and give ORS.
2.Give zinc medicine
Give zinc 10 days in a row even though the diarrhea has stopped. Can be given by
chewing or dissolved in 1 tablespoon of boiled water or breast milk.
- Age < 6 months given 10 mg (1/2 tablet) per day
- Age > 6 months given 20 mg (1 tablet) per day.
3.Feed children to prevent malnutrition

• Feed according to the child's age with the same menu when the child is healthy
• Add 1-2 teaspoons of vegetable oil per serving
• Give foods rich in Potassium such as fresh fruit juice, bananas, green coconut water.
• Feed more often than usual with smaller portions (every 3-4 hours)
• After the diarrhea stops, give the same food and additional food for 2 weeks
4.Advise mother/caregiver
To bring the child back to the health worker if:
• Watery stools more often

• Repeated vomiting
• Very thirsty
• Eat and drink very little
• Fever occurs
• Bloody stools
• Not getting better in 3 days
2. Mild/moderate dehydrated diarrhea: If there are two or more signs

- Nervous,fussy
- Boy eyes
- Want to drink constantly, there is thirst
- Stomach skin pinch/turgor Returns slowly
Treatment Plan B: For the treatment of mild to moderate dehydration diarrhea
The amount of ORS given in the first 3 hours at the health facility
ORS given =
75 ml x child's WEIGHT
• If the BB is unknown, give ORS according to the table below:
Age Up 4 months 4 -12 12-24 2-5 years

months month
s
Weight < 6 kg 6-10 kg 10-12 12-19 kg
kg
Liquid 200-400 400-700 700- 900-1400
amount 900
• If the child wants more ORS, give it.
• Persuade the mother to continue breastfeeding.
• For infants < 6 months who are not breastfed, also give 100-200 ml of boiled water during
this time.
• For children > 6 months, delay feeding for 3 hours except breast milk and ORS
• Give Zinc medicine for 10 consecutive days
Observe the child closely and help the mother give ORS:
- Indicate the amount of fluid to be given.
- Give little by little but often from a glass.
- Check from time to time if there is a problem.
- If the child's eyelids are swollen, stop giving ORS and give boiled water or breast
milk. Give ORS according to Treatment Plan A when the swelling has
disappeared.
AFTER 3-4 HOURS, ASSESS THE CHILD AGAIN USING THE SCREENING
CHART, THENSELECT THERAPY PLAN A, B OR C TO CONTINUE
THERAPY
• If there is no dehydration, switch to Treatment Plan A. When the dehydration has

disappeared, the child usually urinates and becomes sleepy and sleeps.
• If signs indicate mild/moderate dehydration, repeat Treatment Plan B
• Children began to be given food, milk and fruit juice.
• If signs indicate severe dehydration, switch to Treatment Plan C
Parenteral administration of fluids and electrolytes is only for cases of severe dehydration.
1. Treatment of diarrhea without dehydration TRO (Oral Rehydration Therapy)
Sufferers of diarrhea without dehydration should be immediately given household
fluids to prevent dehydration, such as: starch water, salt-sugar solution, vegetable
gravy and so on. Treatment can be done at home by the patient's family. The
amount of fluid given is 10 ml/kg BW or for children aged < 1 year is 50-100 ml,
1-5 years is 100-200 ml, 5-12 years is 200-300 ml and adults is 300-400 ml for
each bowel movement . For children under 2 years of age, liquids should be given
by spoon at a rate of 1 spoon every 1 to 2 minutes. Bottle feeding is not permitted.
Older children can drink directly from a cup or glass with frequent sips. If vomiting
occurs, stop for 10 minutes then start again slowly, for example 1 spoon every 2-3
minutes.
2. Treatment of mild to moderate dehydration diarrhea: TRO (Oral Rehydration
Therapy) Diarrhea sufferers with mild to moderate dehydration should be treated at
a health facility and immediately given oral rehydration therapy with ORS. The
amount of ORS given for the first 3 hours is 75 cc/kg. If the body weight is not
known, even though this method is not precise, estimates of fluid deficiency can be
determined using the patient's age, namely: for ages < 1 year is 300 ml, 1-5 years is
600 ml, > 5 years is 1200 ml and adults is 2400 ml. This range of fluid volume
values is approximate; the volume actually administered is determined by assessing
the patient's thirst and monitoring for signs of dehydration. If the patient is still
thirsty and still wants to drink, it should be given again. Conversely, if the volume
above the eyelids becomes swollen,
3. Treatment of severe dehydrated diarrhea TRP (Parenteral Rehydration Therapy)
Sufferers of severe dehydrated diarrhea must be treated at a health center or
hospital. The best treatment is parenteral rehydration therapy. Patients who are able
to drink even a small amount should be given ORS until IV fluids are installed. In
addition, all children should be given ORS during administration of intravenous
fluids (5 ml/kg/hour), if you can drink well, usually in 3-4 hours (for babies) or 1-
2 hours (for older children). The administration is done to provide additional base
and potassium which may not be supplied sufficiently by administering intravenous
fluids. For parenteral rehydration, Lactate Ringer's solution is used at a dose of 100
ml/kg BW. The method of administration for < 1 year the first hour is 30 cc/kgBB,
followed by the next 5 hours 70 cc/kgBB. Over 1 year 1/2 hour first 30 cc/kgBB
continued 2 ½ hours later 70 cc/kgBB. Do an hourly evaluation. If hydration does
not improve, IV drip can be sped up. After 6 hours in infants or 3 hours in older
children, evaluate, choose the next appropriate treatment, namely: treatment of
diarrhea with mild moderate dehydration or treatment of diarrhea without
dehydration. 30 4. Oral Rehydration Liquid (CRO) In 1975 WHO and Unicef
agreed to promote a single CRO containing (in mmol/L) Sodium 90, Potassium 20,
Chloride 80, Base 30 and Glucose 111 (2%). This composition was chosen to allow
a single type of solution to be used in the treatment of diarrhea caused by various
infectious agents accompanied by varying degrees of electrolyte loss. Examples of
Rotavirus diarrhea are associated with loss of sodium with feces of 30 – 40 mEq/L,
ETEC 50 – 60 mEq/L and V. cholera > 90 – 120 mEq/L. 18 This composition was
chosen to allow a single type of solution to be used in the treatment of diarrhea
caused by various infectious agents accompanied by varying degrees of electrolyte
loss. Examples of Rotavirus diarrhea are associated with loss of sodium with feces
of 30 – 40 mEq/L, ETEC 50 – 60 mEq/L and V. cholera > 90 – 120 mEq/L. 18
This composition was chosen to allow a single type of solution to be used in the
treatment of diarrhea caused by various infectious agents accompanied by varying
degrees of electrolyte loss. Examples of Rotavirus diarrhea are associated with loss
of sodium with feces of 30 – 40 mEq/L, ETEC 50 – 60 mEq/L and V. cholera > 90
– 120 mEq/L. 18
4. Zinc (Zinc)
Zinc deficiency is common in children in developing countries and is associated
with reduced immune function and an increased incidence of serious infectious
diseases. Zinc is a micronutrient component of various enzymes in the body, which
is important, among others, for DNA synthesis. In a systematic review of 10 RCTs,
all conducted in developing countries in 1999, it was found that zinc
supplementation at a dose of at least half of the United States RDA for zinc reduced
the incidence of diarrhea by 15% and the prevalence of diarrhea by 25%, more or
less the same as the results achieved by other preventive measures such as
improved sanitation hygiene and breastfeeding
5. Medical therapy
Various drugs have been used for the treatment of diarrhea such as:
antibiotics, antidiarrheals, adsorbents, antiemetics and drugs that affect the
intestinal microflora. Some drugs have more than one mechanism of
action, many of which have systemic toxic effects and most are not
recommended for children younger than 2-3 years. It is generally said that
these drugs are not necessary for the treatment of acute diarrhea.
Antibiotics Antibiotics are generally not needed in all acute diarrhea
because most infectious diarrhea is rotavirus which is self-limited and
cannot be killed with antibiotics. Only a small proportion (10 – 20%) are
caused by pathogenic bacteria such as V. cholera, Shigella,
Enterotoxigenic E. coli, Salmonella, Camphylobacter and so on17.
Table 15. antibiotics in diarrhea

3.2.7 Complications
Several problems may occur during rehydration treatment. Some of

them require special treatment, electrolyte disturbances:19
 Hypernatremia
Patients with diarrhea with plasma sodium > 150 mmol/L require
close periodic monitoring. The goal is to slowly lower sodium levels. A
rapid decrease in plasma sodium levels is very dangerous because it can
cause brain edema. Oral or nasogastric rehydration using ORS is the best
and safest way. Correction with intravenous rehydration can be done using
0.45% saline – 5% dextrose for 8 hours. Calculate fluid requirements using
body weight without correction. Check plasma sodium level after 8 hours.
If normal continue with maintenance, if otherwise continue for another 8
hours and check plasma sodium again after 8 hours. For maintenance use
0.18% saline - 5% dextrose, calculated for 24 hours. Add 10 mmol KCl for
every 500 ml of infusion after the patient is able to urinate. Then the
normal diet can be started. Continue giving ORS 10 ml/kg/each bowel
movement, until the diarrhea stops. Hyponatremia Children with diarrhea
who only drink water or fluids containing only a small amount of salt, may
develop hyponatremia (Na < 130 mol/L).
 Hyponatremia
It occurs frequently in children with shigellosis and in severely
malnourished children with oedema. ORS is safe and effective for the
treatment of nearly all children with hyponatremia. If that doesn't work, Na
correction is carried out together with rehydration fluid correction, namely:
using Lactate Ringer's or Normal Saline. Corrected Na level (mEq/L) =
125 – serum Na level examined multiplied by 0.6 and multiplied by body
weight. Half given in 8 hours, the rest given in 16 hours. The increase in
serum Na should not exceed 2 mEq/L/hour. Hyperkalemia Called
hyperkalemia if K > 5 mEq/L, correction is made by administering 10%
calcium gluconate 0.5 – 1 ml/kg BW iv slowly over 5 – 10 minutes with a
heart rate monitor.
 hypokalemia
It is said to be hypokalemia if K < 3.5 mEq/L, correction is made
according to K levels: if potassium is 2.5 – 3.5 mEq/L given orally 75
mcg/kgBW/day divided into 3 doses. If < 2.5 mEq/L then given intravenous
drip (no bolus) given within 4 hours. The dose: (3.5 – measured K x BW x 0.4
+ 2 mEq/kgBW/24 hours) given in 4 hours, then another 20 hours (3.5 –
measured K x BW x 0.4 + 1/6 x 2 mEq x BB). Hypokalemia can cause muscle
weakness, paralytic ileus, impaired kidney function and cardiac arrhythmias.
Hypokalemia can be prevented and potassium deficiency corrected by using
ORS and giving potassium-rich foods during and after the diarrhea has
stopped.
3.2.8 Prevention
Efforts to prevent diarrhea can be done by: 17
1. Prevent the spread of pathogenic germs that cause diarrhea. Pathogenic

germs that cause diarrhea are generally spread by faecal-oral. Stopping the
spread of germs that cause diarrhea needs to be focused on this way of
spreading. Efforts to prevent diarrhea that have proven effective include:
a. Proper breastfeeding.
b. Improving the preparation and storage of complementary foods for
breast milk.
c. Adequate use of clean water.
d. Cultivating the habit of washing hands with soap after defecating and
before eating.
e. Use of clean and hygienic latrines by all family members. Correct
disposal of baby stools.
2. Improve the host's immune system. Ways that can be done to increase the
child's immune system and reduce the risk of diarrhea include: 17
a. Give breast milk at least until the age of 2 years.
b. Increase the nutritional value of complementary foods and provide
sufficient amounts of food to improve the nutritional status of children.
c. Measles immunization.
3.3 Pleural effusion
3.3.1 Definition
Pleural effusion is a condition where there is a buildup of fluid in the

pleural space. The effusion may be a clear fluid, which may be a transudate,
exudate, or it may be blood or pus. Pleural effusion is a condition in which there is
accumulation of fluid in the pleural space in the form of transudate and exudate
resulting from an imbalance between production and absorption in the capillaries
and visceral pleura. According to (Joyce M. Black, 2014) Pleural effusion is a
buildup of fluid in the pleural cavity. Pleural fluid normally seeps continuously
into the chest cavity from the capillaries lining the parietal pleura and is
reabsorbed by the capillaries and lymphatic system of the visceral pleura. Any
condition that interferes with the secretion or drainage of this fluid will cause a
pleural effusion.
3.3.2 Anatomy and physiology of the Pleura
Pleura is a complementary structure of the respiratory system that

functions as a supporting structure needed in the process of running the
respiratory system. Other complementary structures, namely the chest wall
which is composed of ribs and muscles, abdominal muscles, diaphragm
and pleura itself.
1. Pleura Anatomy
The pleura is a serous membrane that lines the inner surface of
the thoracic wall on the right and left, lines the superior surface of the
right and left diaphragm, lines the right and left mediastinum (all of
which are called the parietal pleura), then at the base of the lung, this
serous membrane reverses lining the lung (pleura visceral) The visceral
pleura may invaginate following the dividing fissures in each lobe of the
lung.
a. Pleura visceralis
The visceral pleura is the pleura that is on the surface of the lung,
consisting of a single layer of thin mesothelial cells < 30µm which is
located on the outer surface. There are lymphocyte cells that are between
the gaps. The endopleura, which contains fibrocytes and histiocytes, is
beneath the mesothelial cells, and underneath is a middle layer of
collagen tissue and elastic fibers. Meanwhile, in the lowest layer there is
subpleura interstitial tissue, which contains many capillaries in it
b. Parietal Pleura
Parietal pleura, namely the pleura which is adjacent to the
thoracic wall, has thicker tissue composed of mesothelial cells and also
composed of connective tissue such as collagen and elastic. Meanwhile,
if the connective tissue is composed of many capillaries from the
intercostals and internal mammaries, in the lymph vessels there are many
sensory nerve receptors that are very sensitive to pain stimuli and also
temperature differences. All of which are composed of intercostalis on
the chest wall and the flow will also match the chest dermatome. So that
it can make it easier for the chest wall that is above it to attach and
detach. So that it functions to produce pleural fluid.
The two layers of the pleura are interconnected by the hilus

pulmonalis which functions as a liaison for the pleura (pulmonary
ligament). In this pleural layer there is a cavity called the pleural cavity.
The pleural cavity has a small amount of pleural fluid which functions to
avoid friction between the pleura when carrying out the breathing process
Figure: 3.2 Anatomy of Pleural Effusion (Sugeng Bambang, 2011)
2. Pleural Physiology
The pleura has a mechanical function, which is to continue the
negative pressure of the thorax to the area of the lungs, so that the lungs can
expand because they are elastic. At rest (resting pressure) the H2O pressure
in the pleura is about -2 to -5 cm, slightly more negative at the apex when
standing. On inspiration the negative pressure in the pleura increases to -25
to -35 H2O. In addition to the mechanical function, the pleural cavity is
sterile because the mesothelial is able to work to phagocytize foreign bodies
and the fluid in the pleural cavity that is produced acts as a lubricant.
The fluid in the pleural cavity is very small, about 0.3 ml/kg, is
hypochotic with a protein concentration in the fluid of about 1 g/dl.
Production and reabsorption of fluid in the pleural space is also likely to be
influenced by respiratory movements and lung gravity. The site of
reabsorption occurs in the parietal pleural lymph vessels at a rate of 0.1 to 0.5
ml/kg/hour. If there is a production and reabsorption disorder, it will result in
pleural effusion.
3.3.3 Etiology
According to Darmanto (2016), there are several factors that cause pleural
effusion as follows: 21
3.3.3.1 Transudative Pleural Effusion

Transudative pleural effusion is a pleural effusion of the type of
transudate effusion. Transudative pleural effusion can be caused by various
factors, including congestive heart failure, pulmonary embolism, liver cirrhosis
or intra-abdominal disease, peritoneal dialysis, hypoalbuminemia, nephrotic
syndrome, acute glomerulonephritis, salt retention and after cardiac surgery.
1. Exudative Pleural Effusion

Exudative pleural effusion is a type of exudate fluid that occurs due to
inflammation or infiltration of the pleura or tissues adjacent to the pleura.
In addition, damage to the capillary walls can also result in the formation
of fluid containing a lot of protein out of the blood vessels and collects in
the pleural space. The cause of exudative pleural effusion can also be
caused by a dam in the lymph vessels.
Other causes of exudative pleural effusion include neoplasms, infections,

connective tissue diseases, intra-abdominal and immunologic diseases.
a. Neoplasm
Neoplasms can cause pleural effusion due to bronchogenic carcinoma
due to the high number of leukocytes in that condition
>2,500/mL. which consists of lymphocytes, malignant cells, and

reaccumulation often occurs after acentesis, besides that metastatic
tumors originating from mammary carcinoma are more often bilateral
compared to bronchogenic carcinoma due to blockage of lymph
vessels or their spread to the pleural area. Other causes are lymphoma,
mesothelioma and benign ovarian tumors or meig syndrome.
b. Infection
The cause of exudative pleural effusion is infection, the
microorganisms are viruses, bacteria, mycoplasma and mycobacteria.
Bacteria from acute pneumonia can rarely cause exudative pleural
effusions, pleural effusions containing pus accompanied by
microorganisms are called empyema. In addition to empyema
pneumonia caused by viruses and mycoplasma can also cause pleural
effusions.
c. Connective tissue disease

Connective tissue diseases that can cause pleural effusion include
systemic lupus erythematosus and rheumatoid arthritis.
d. Intra-abdominal disease
Pleural effusions caused by intra-abdominal disease can not only
cause exudative pleural effusions but can also cause transudative
pleural effusions depending on the type of cause. Intra-abdominal
diseases that can cause exudative pleural effusion are cases of post-
abdominal surgery, intestinal perforation, and hepatobiliary which can
cause subdiaphragmatic abscesses. The thing that is often found as a
cause of pleural effusion from intra-abdominal disease is hepatic
abscess due to amoeba
e. Immunologic
Immunologics that can cause pleural effusions are such as rheumatoid
effusion, lupus effusion, sarcoidotic effusion, Wagner's
granulomatosis, Sjogren's syndrome, post-cardiac injury, pulmonary
embolism, uremic lung and Meig's syndrome.
Rheumatoid pleural effusion is more common in male patients than in

female patients. Usually, moderate to severe rheumatoid patients who
have subcutaneous nodules can develop rheumatoid pleural effusion.
In patients with rheumatoid pleural effusion, patients complain of
pleuritic pain and shortness of breath.
2. Hemorrhagic pleural effusion

Hemorrhagic pleural effusion is a pleural effusion caused by trauma,
tumor, lung infarction or tuberculosis.
3. Based on the location of the liquid formed

The causes of pleural effusion from the site of formation can be divided
into two parts, namely unilateral and bilateral. The type of unilateral
pleural effusion has nothing to do with the cause of the disease but bilateral
pleural effusion can be found in the following diseases such as congestive
heart failure, nephrotic syndrome, ascites, lung infarction, tumors and
tuberculosis.
4. Pleural fluid analysis

According to Dramano (2016), the analysis of pleural fluid is as follows.
Pleural fluid is examined macroscopically for color, turbidity, and odor of
the fluid. Transudate pleural effusions are usually clear, transparent, straw-
yellow in color and odorless. While the fluid from the pleura that
resembles milk
3.3.4 Clinical Manifestations
According to Saferi & Mariza (2013), signs and symptoms arising from pleural
effusion based on the cause are:23
a. Hard to breathe
b. Heaviness in the chest area
c. Heart murmurs caused by heart failure
d. Progressive weakness
e. Weight loss due to neoplasm
f. Cough with blood in smokers caused by bronchial cancer
g. Subfebrile fever caused by pulmonary TB
h. Fever chills caused by empyema
i. Ascites in patients with cirrhosis of the liver
j. Ascites accompanied by a tumor in the pelvic area caused by a sufferer of
Meig's syndrome.
3.3.5 Management
According to Herdman Kamitsuru (2011), nursing actions that can be performed

on clients with pleural effusion include:22
a. Position the client in a semi-Fowler's position

Namely with a half-sitting position with a 45o position which aims to
provide a sense of comfort.
b. Do deep breathing exercises

Which aims to free from interference ventilation
c. Monitor breathing patterns, additional breath sounds, rate, depth and

difficulty with breathing.
d. Collaborating on drug therapy
If the causative agent of pleural effusion is a germ or bacteria, antibiotics
can be used.
e. Percuss the chest anteriorly and posteriorly from the apex to the base
of the lung.
f. Monitor the patient's shortness of breath, including activities that can
increase the patient's shortness of breath.
3.3.6 Pathophysiology
The location of the visceral pleura and perietal pleura face each other and
are only separated by a thin membrane of serous fluid, this fluid layer shows a
balance between transudation and pleural capillaries and absorption by the
viscelar and parietal veins and also lymph channels. Because pleural effusion is a
collection of excess fluid in the pleural cavity in the visceral and parietal pleural
cavities, this problem can cause expansion of the lungs and cause the patient to
breathe rapidly (tachypnea) so that oxygen can be obtained optimally. From this
problem, the client experiences interference in the effectiveness of his breathing
pattern. Ineffective breathing pattern is a condition in which the patient
experiences a decrease in actual or potential ventilation caused by a change in
breathing pattern. Generally these cases are established on the diagnosis of
hyperventilation. Ineffective breathing pattern is characterized by dyspnea,
tachypnea, changes in the depth of breathing, cyanosis and changes in chest wall
movement.
Pleural effusion can be exudate or transudate. Transudate can be caused

if there is an increase in pulmonary venous pressure, for example in patients with
congestive heart failure. Power balance causes discharge of fluid from vessels
Transudation can also cause hypoproteinemia as in liver and kidney disease. If
the pleural effusion contains pus, it is called an empyema. Empyema is caused by
extension of infection from adjacent structures and is a complication of
pneumonia, lung abscess or perforation of carcinoma into the pleural space. If the
empyema is not treated with drainage, it will endanger the thoracic wall. Exudate
due to inflammation will undergo organization and fibrous attachment occurs
between the visceral and parietal pleura, which is called a fibrothorax.
3.3.7 Supporting investigation
According to Darmanto (2016), supporting examinations that can be

carried out in patients with pleural effusion include the following:
3.3.7.1 X-ray overview

Abnormalities on a PA X-ray will only be seen if the
accumulation of pleural fluid reaches 300 mL. Initially, fluid collects at
the base of the hemithorax between the inferior surface of the lung and
the diaphragm, especially posteriorly, namely the deep pleural sinuses. If
the pleural fluid continues to increase in number, the fluid will go up,
namely to the concave lung area and reach the top. The diaphragm and
costophrenic sinuses will not be seen if the pleural fluid reaches 1000
mL. if the PA photo of the pleural effusion looks unclear, a lateral
decubitus photo can be done.
3.3.7.2 pH chemistry check

In addition to microscopic and cytological examinations carried
out, other examinations are chemical and pH examinations. What is
checked is glucose, amylase and other enzymes.
3.3.8 Complications
3.3.8.1 Fibrothorax
Exudative pleural effusion that cannot be handled properly by
drainage measures will cause fibrous adhesions between the visceral
pleura and parietal pleura. If the fibrothorax expands it can cause severe
mechanical resistance to the underlying tissues and surgery must be done
immediately.
3.3.8.2 Atelectasis
Atelectasis is an incomplete development of the lungs caused by
pressure due to pleural effusion.
3.3.8.3 Fibrosis
Pulmonary fibrosis is a pathological condition in which there is
an excessive amount of lung connective tissue. Fibrosis can arise due to
the process of tissue repair as a continuation of a lung disease that causes
inflammation. In prolonged atelectasis pleural effusion can also cause
replacement of new tissue that is attacked by fibrous tissue.

Dengue Hemorrhagic Fever

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DENGUE HEMORRHAGIC FEVER

Dengue hemorrhagic fever (DHF) is more common in children under 15 years of

Expanded dengue syndrome is an unusual manifestation that is increasingly being

Undifferentiated fever Undifferentiated fever is a fever in infants, children and adults

Bleeding manifestations: skin bleeding may be seen as a positive tourniquet test

3.1.4. Illness Course

Figure 2. The course of dengue infection.

Table 1. Differential Diagnosis of Dengue in the Fever Phase

Dengue-like condition in the Fever Phase

Mild bleeding manifestations such as

The critical phase occurs when the fever

The appearance of warning signs is a

In these patients there was a very rapid increase

Table 2. Differential diagnosis of dengue in the critical phase

Dengue-like condition in Critical Phase

Warning signsgenerally occurs towards the end of the

Every time you find a patient with fever with

Setting clear definitions for warning signs and the severity

Table 3. Warning signs

Parameter Description Explanation

Pleural effusion and ascites can be detected

Persistent vomiting and severe abdominal pain

If the patient survives the critical phase within

is redundantly rendered in Figure 3.

Figure 3. Clinical problems during the dengue disease course

3.1.5 Classification of Dengue Infection

A prospective multicenter clinical study in a

a) Dengue without warning signs.

Figure 4. Classification of Dengue Infection

Dengue severity classification can be used practically

Severe dengue cases in Southeast Asia occupy

Increased vascular permeability is followed by severe

Parameter Circulati Compensated Shock Decompensated

Parameter Circulation Compensated Decompensated

Explanation of the normal values of

Age Normal Normal Normal Normal MAP

To recognize shock, when examining patients with

Figure 5. The “5-in-1 maneuver” magic touch–CCTV-R

The patient is said to be in shock if the pulse pressure

a. There is evidence of plasma leakage such as a rapidly

d. There is a change in consciousness (lethargy or

f. There is severe organ damage (acute liver failure,

Further explanation regarding the definition of shock

1) Poor capillary perfusion is characterized by

3) Hypotension or until immeasurable.

4) The pulse feels weak and small until it can't be felt.

A decrease in systolic blood pressure >40 mm Hg or

c. Respiratory distress (shortness of breath):

1) Respiratory rate increases with age.

2) Increased work of breathing (dyspnea).

4) Saturation 02 ≤94% without administration 02.

e. Involvement of the central nervous system, in the form of:

1) Decreased consciousness without finding

f. Renal involvement, in the form of:

1) Serum creatinine ≥2x compared to the upper limit of normal

2) Serum creatinine >1.2 mg/dL.

Assessment of AKI using the criteria of pediatric

g. Liver involvement, in the form of:

1) Fail heart I which be marked with