Dengue is a systemic and dynamic disease with a wide spectrum of clinical presentations that range

from mild to severe;however, the clinical evolution and outcomemay be highly unpredictable.The
course of illness is characterized by three well-demarcated phases: febrile;critical; and recovery
(2). Although most patients recover after a self-limiting, nonsevere,clinical course, a small
proportion progress to have severe disease, which ischaracterized by plasma leakage with or
without hemorrhage (2).
Clinical Phases of Dengue. After theincubation period, the illness begins abruptly and is followed
by the three phases (Fig. 3). Phase 1: The febrile phase. Typically, a patient develops a high-grade
fever that lasts 2–7 days and is acutely unwell with headache, diffuse erythema, generalized
myalgia, and arthralgia; anorexia, nausea, and vomiting are also common. Younger children may
develop febrile seizures. It may be difficult to distinguish dengue clinically from other viral fevers,
although demonstration of microvascular fragility by a positive tourniquet-test result increases the
likelihood that it is dengue (2). Frequent meticulous monitoring for warning signs and other
clinical parameters (Fig. 2) is crucial for recognizing progression to the critical phase. Although a
tender hepatomegaly and mild hemorrhagic manifestations (petechiae and mucous membrane
bleeding from nasal or oral cavity) may be seen often, significant bleeding episodes from the
gastrointestinal tract or menorrhagia are uncommon occurrences in the febrile phase. The earliest
laboratory abnormality is a progressive leukopenia, which is another clue to the presence of
probable dengue.
Phase 2: The critical phase. The critical phase begins around the period of defervescence, when
several important occurrences mark their presence in quick succession. Leukopenia progresses
further, and a rapid decrease in platelet count usually occurs. This precedes the most specific and
life-threatening manifestation of this phase: an increase in capillary permeability that leads to
plasma leakage and an equivalent rise in hematocrit (Hct). Plasma leakage begins during the febrile
phase, but at a time when the viral load and body temperature are declining, and develops rapidly
over a period of hours. The period of plasma leakage is short-lived, typically lasting 24–48 hrs.
However, the extent of plasma loss is highly variable and is the key that determines the clinical
severity in the critical phase (i.e., whether the patient recovers uneventfully, develops dengue with
warning signs, or, in a small proportion with extensive plasma leak, progresses to have “severe
dengue”). ome patients with a nonsevere form of dengue do not develop plasma leak and steadily
improve after defervescence. Prolonged uncorrected shock, metabolic acidosis, and
thrombocytopenia may worsen disseminated intravascular coagulation, which may, in turn, lead
to massive hemorrhage, thus setting off a progressive downward spiral of worse shock and
hemorrhage (1, 11, 12, 29); these patients are at high risk of death. Apart from shock and
hemorrhage, other important consequences of increased capillary permeability are
hemoconcentration, hypoalbuminemia, and serous fluid collections, usually pleural effusions and
ascites, the extent of which depends both on the magnitude of plasma leak and the volume of fluids
consumed or prescribed (1, 2). Early confirmation of plasma leakage in the critical phase may be
provided by serial laboratory studies with complete blood counts demonstrating the triad of
progressively increasing Hct, leukopenia, and thrombocytopenia, ultrasound findings of a
thickened gall bladder wall, and ascitic and pleural fluid and chest radiograph showing pleural
effusions (1, 2). These findings are useful for triage and therapy because they may be present much
earlier than signs of plasma loss are clinically manifest and also indicate progress to the critical
phase in patients who do not defervesce despite the onset of plasma leakage (2, 11, 12). Evaluating
hemoconcentration in patients with preexisting anemia may be difficult, because the preillness Hct
level may be unavailable at the time of admission. Using the population baseline may be useful
(2), such as a cutoff Hct value (36%) in Indian children due to the high prevalence of iron-
deficiency anemia (30). Phase 3: The recovery phase. After the critical 24–48 hrs of plasma
leakage, the final recovery phase is heralded by the gradual resorption of the leaked plasma back
into the intravascular compartment over the next 48–72 hrs. The patient may exhibit dramatic
improvement with an overall sense of well-being, improved appetite, a stable hemodynamic
status, and a brisk diuresis. Pruritis and an asymptomatic bradycardia may be marked (1, 2). The
blood picture reflects the recovery phase with a lower Hct level on account of the reabsorbed fluid
and a white cell increment that may precede platelet recovery. Recognition of this phase is
important so that intravenous (IV) fluids may be promptly ceased. This simple intervention may
prevent fluid overload (FO), which, along with severe hemorrhage, is an important, preventable
cause of death by dengue (Fig. 3)