We continue our Back to College Series on Dengue Fever bringing to you a detailed MD curated article on the Signs and Symptoms of Dengue Fever. On average, dengue becomes symptomatic after a 4- to 10-day incubation period (range, 3-14 days). Dengue symptoms usually last 2-7 days.
Many individuals with dengue may be asymptomatic. Many patients with dengue experience a prodrome of chills; rash, including erythematous mottling of the skin; and facial flushing, which may last 2-3 days.
Children younger than 15 years who have dengue usually have a nonspecific febrile syndrome, which may be accompanied by a maculopapular rash. Dengue should be suspected in individuals who present with high fever (104°F/40°C), retro-orbital headache, muscle and joint pain, nausea, lymphadenopathy, vomiting, and rash and who have traveled within two weeks of symptom onset to an area where appropriate vectors are present and dengue transmission may be occurring.
Accompanying symptoms in patients with dengue may include any of the following:
- Retro-orbital pain
- Severe myalgias: Especially of the lower back, arms, and legs
- Arthralgias: Usually of the knees and shoulders
- Nausea and vomiting (diarrhoea is rare)
- Rash: A maculopapular or macular confluent rash over the face, thorax, and flexor surfaces, with islands of skin sparing
- Weakness, malaise, and lethargy
- Altered taste sensation
- Sore throat
- Mild hemorrhagic manifestations (e.g., petechiae, bleeding gums, epistaxis, menorrhagia, haematuria)
Rash in dengue fever is a maculopapular or macular confluent rash over the face, thorax, and flexor surfaces, with islands of skin sparing. The rash typically begins on day 3 and persists 2-3 days.
Fever typically abates with the cessation of viremia. Occasionally, and more commonly in children, the fever abates for a day and then returns, a pattern that has been called saddleback fever. A second rash may occur within 1-2 days of effervescence, lasting 1-5 days; it is morbilliform, is maculopapular, spares the palms and soles, and occasionally desquamates.
Recovery is complete but slow, with fatigue and exhaustion often persisting after the fever has subsided. The convalescent phase may last for two weeks.
Clinical course of dengue fever
Patients typically develop high-grade fever suddenly. This acute febrile phase usually lasts 2–7 days and is often accompanied by facial flushing, skin erythema, generalized body ache, myalgia, arthralgia, and headache. Some patients may have a sore throat, injected pharynx, and conjunctival injection. Anorexia, nausea, and vomiting are common.
It can be difficult to distinguish dengue clinically from non-dengue febrile diseases in the early febrile phase. A positive tourniquet test in this phase increases the probability of dengue. Also, these clinical features are indistinguishable between severe and non-severe dengue cases.
Therefore, monitoring for warning signs and other clinical parameters is crucial to recognizing progression to the critical phase. Mild hemorrhagic manifestations like petechiae and mucosal membrane bleeding (e.g., nose and gums) may be seen.
Massive vaginal bleeding (in women of childbearing age) and gastrointestinal bleeding may occur during this phase but is not common. The liver is often enlarged and tender after a few days of fever.
The earliest abnormality in the full blood count is a progressive decrease in total white cell count, which should alert the physician to a high probability of dengue.
Around the time of defervescence, when the temperature drops to 37.5–38 C or less and remains below this level, usually on days 3–7 of illness, an increase in capillary permeability in parallel with increasing hematocrit levels may occur. This marks the beginning of the critical phase. The period of clinically significant plasma leakage usually lasts 24–48 hours.
Progressive leukopenia followed by a rapid decrease in platelet count usually precedes plasma leakage. At this point patients without an increase in capillary permeability will improve, while those with increased capillary permeability may become worse because of lost plasma volume.
The degree of plasma leakage varies. Pleural effusion and ascites may be clinically detectable depending on the degree of plasma leakage and the volume of fluid therapy. Hence chest x-ray and abdominal ultrasound can be useful tools for diagnosis. The degree of increase in the baseline hematocrit often reflects the severity of plasma leakage.
Shock occurs when a critical volume of plasma is lost through leakage. It is often preceded by warning signs. The body temperature may be subnormal when a shock occurs.
With a prolonged shock, the consequent organ hypoperfusion resulted in progressive organ impairment, metabolic acidosis and disseminated intravascular coagulation. This in turn leads to severe hemorrhage causing the hematocrit to decrease in severe shock. Instead of the leukopenia.
If the patient survives the 24–48-hour critical phase, a gradual reabsorption of extravascular compartment fluid takes place in the following 48–72 hours. General well-being improves, appetite returns, gastrointestinal symptoms abate, hemodynamic status stabilizes, and diuresis ensues. Some patients may have a rash of “isles of white in the sea of red ‘’ it is seen when individual maculopapular /morbilliform rash coalesced and seen as general congruent erythema with petechiae and rounded islands of sparing -White Island in a sea of red (thought to be due to an immune response).”
Some may experience generalized pruritus. Bradycardia and electrocardiographic changes are common during this stage. The hematocrit stabilizes or may be lower due to the dilutional effect of reabsorbed fluid. White blood cell count usually starts to rise soon after defervescence, but the recovery of platelet count is typically later than that of white blood cell count.
Respiratory distress from massive pleural effusion and ascites will occur at any time if excessive intravenous fluids have been administered. During the critical and recovery phases, excessive fluid therapy is associated with pulmonary edema or congestive heart failure.
The various clinical problems during the different phases of dengue can be summarized:
Febrile phase | Dehydration; high fever may cause neurological disturbances and febrile seizures in young children.
2 Critical phases | Shock from plasma leakage; severe hemorrhage; organ impairment.
3 Recovery phases | Hypervolemia (only if intravenous fluid therapy has been excessive and has extended into this period).
(Dengue Hemorrhagic Fever and Dengue Shock Syndrome)
Severe dengue is defined by one or more of the following:
- Plasma leakage that may lead to shock (dengue shock) and fluid accumulation, with or without respiratory distress,
- and (ii) severe bleeding,
- and (iii) severe organ impairment.
As dengue vascular permeability progresses, hypovolaemia worsens and results in shock. It usually takes place around defervescence, usually on day 4 or 5 (range days 3–7) of illness, preceded by the warning signs. During the initial stage of shock, the compensatory mechanism which maintains a normal systolic blood pressure also produces tachycardia and peripheral vasoconstriction with reduced skin perfusion, resulting in cold extremities and delayed capillary refill time. Uniquely, the diastolic pressure rises towards the systolic pressure and the pulse pressure narrows as the peripheral vascular resistance increases.
Patients in dengue shock often remain conscious and lucid. The inexperienced physician may measure a normal systolic pressure and misjudge the critical state of the patient. Finally, there is decompensation and both pressures disappear abruptly. Prolonged hypotensive shock and hypoxia may lead to multi-organ failure and an extremely difficult clinical course. The patient is considered to have shock if the pulse pressure (i.e. the difference between the systolic and diastolic pressures) is ≤ 20 mm Hg in children or he/she has signs of poor capillary perfusion (cold extremities, delayed capillary refill, or rapid pulse rate). In adults, the pulse pressure of ≤ 20 mm Hg may indicate a more severe shock.
Hypotension is usually associated with prolonged shock which is often complicated by major bleeding. Patients with severe dengue may have coagulation abnormalities, but these are usually not sufficient to cause major bleeding. When major bleeding does occur, it is almost always associated with profound shock since this, in combination with thrombocytopaenia, hypoxia and acidosis, can lead to multiple organ failure and advanced disseminated intravascular coagulation. Massive bleeding may occur without prolonged shock in instances when acetylsalicylic acid (aspirin), ibuprofen or corticosteroids have been taken.
Unusual manifestations, including acute liver failure and encephalopathy, may be present, even in the absence of severe plasma leakage or shock. Cardiomyopathy and encephalitis are also reported in a few dengue cases. However, most deaths from dengue occur in patients with profound shock, particularly if the situation is complicated by fluid overload.
Severe dengue should be considered if the patient is from an area of dengue risk presenting with fever of 2–7 days plus any of the following features:
- There is evidence of plasma leakage, such as:
- High or progressively rising haematocrit
- Pleural effusions or ascites
- Circulatory compromise or shock (tachycardia, cold and clammy extremities, capillary refill time greater than three seconds, weak or undetectable pulse, narrow pulse pressure or, in late shock, unrecordable blood pressure).
- There is significant bleeding.
- There is an altered level of consciousness (lethargy or restlessness, coma, convulsions
- There is severe gastrointestinal involvement (persistent vomiting, increasing or intense abdominal pain, jaundice)
- There is severe organ impairment (acute liver failure, acute renal failure, encephalopathy or encephalitis, or other unusual manifestations, cardiomyopathy) or other unusual manifestations.
The initial phase of severe dengue is like that of dengue fever and other febrile viral illnesses. Shortly after the fever breaks (3-7 days after symptom onset or sometimes within 24 hours before), signs of plasma leakage appear, along with the development of hemorrhagic symptoms such as bleeding from sites of trauma, gastrointestinal bleeding, and haematuria.
Patients may also present with severe abdominal pain, persistent vomiting that may contain blood, fatigue, and febrile seizures (in children).
The subsequent 24 hours frequently prove critical. If left untreated, hemorrhagic fever most likely progresses to shock. Common symptoms of impending shock include abdominal pain, vomiting, and restlessness.
Patients also may have symptoms related to the circulatory failures, such as pallor, tachypnoea, tachycardia, dizziness/light-headedness, and a decreased level of consciousness.
Dengue Hemorrhagic Fever
Findings for dengue hemorrhagic fever are like those for dengue fever and include the following:
- Biphasic fever curve
- Hemorrhagic findings more pronounced than in dengue fever
- Signs of peritoneal effusion, pleural effusion, or both
Minimal criteria for the diagnosis of dengue hemorrhagic fever, according to the World Health Organization (WHO), are as follows
- Hemorrhagic manifestations (e.g., haemoconcentration, thrombocytopenia, positive tourniquet test)
- Circulatory failure, such as signs of vascular permeability (e.g., hypoproteinaemia, effusions)
Also, conjunctival injection develops in approximately one-third of patients with dengue hemorrhagic fever. Optic neuropathy has been reported and occasionally results in permanent and significant visual impairment.
Pharyngeal injection develops in almost 97% of patients with dengue hemorrhagic fever. Generalized lymphadenopathy is observed.
Hepatomegaly is present more often in dengue shock syndrome than in milder cases. Hepatic transaminase levels may be mild to moderately elevated. Encephalopathy is a rare complication that may result from a combination of cerebral edema, intracranial hemorrhage, anoxia, hyponatremia, and hepatic injury.
Dengue shock syndrome
Findings of dengue shock syndrome include the following:
- Bradycardia (paradoxical) or tachycardia associated with hypovolemic shock
- Narrow pulse pressure (< 20 mm Hg)
- Signs of decreased peripheral perfusion
Dengue can occasionally affect several other body systems either in isolation or along with the classic dengue symptoms. A decreased level of consciousness occurs in 0.5–6% of severe cases, which is attributable either to inflammation of the brain by the virus or indirectly as a result of impairment of vital organs, for example, the liver.
Other neurological disorders have been reported in the context of dengue, such as transverse myelitis and Guillain–Barré syndrome. Infection of the heart and acute liver failure are among the rarer complications.
A pregnant woman who develops dengue may be at a higher risk of miscarriage as well as low birth weight and premature birth.
- Center for Disease Control and Prevention
- National Center for Emerging and Zoonotic Infectious Diseases (NCEZID)
- WHO | Dengue fever and dengue hemorrhagic fever prevention and control. World Health Assembly Resolution WHA55.17, adopted by the 55th World Health Assembly, 2002
- WHO | Revision of the International Health Regulations. World Health Assembly
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