DENGUE- A MANUAL OF CLINICAL DIAGNOSIS..SYAM

Clinical diagnosis

Dengue virus infections may be asymptomatic or may lead to undifferentiated fever, dengue fever (DF) or dengue haemorrhagic fever (DHF) with plasma leakage that may lead to hypovolaemic shock (dengue shock syndrome, DSS)

Dengue fever

The clinical features of DF frequently depend on the age of the patient. Infants and young children may have an undifferentiated febrile disease, often with a maculopapular rash. Older children and adults may have either a mild febrile syndrome or the classic incapacitating disease with high fever of abrupt onset, sometimes with 2 peaks (saddle-backed), severe headache, pain behind the eyes, muscle and bone or joint pains, nausea and vomiting, and rash. Skin haemorrhages (petechiae) are not uncommon. Leukopenia is usually seen and thrombocytopenia may be observed. Recovery may be associated with prolonged fatigue and depression, especially in adults.

In some epidemics, DF may be accompanied by bleeding complications,
such as epistaxis, gingival bleeding, gastrointestinal bleeding, haematuria, and menorrhagia. During outbreaks of DEN-1 infections in Taiwan, China, studies have shown that severe gastrointestinal bleeding may occur in persons with preexisting peptic ulcer disease. Unusually severe bleeding can cause death in such cases. The case-fatality rate of DF, however, is less than 1%. It is important to differentiate cases of DF with unusual bleeding from cases of DHF with increased vascular permeability, the latter being characterized by haemoconcentration. In many endemic areas, DF must also be differentiated from chikungunya fever, another vector-borne virus disease of similar epidemiology and overlapping distribution in much of Asia and the Pacific

Dengue haemorrhagic fever

Typical cases of DHF are characterized by four major clinical manifestations:
1. high fever
2. haemorrhagic phenomena
3. hepatomegaly
4. circulatory failure.


Moderate to marked thrombocytopenia with concurrent haemoconcentration
is a distinctive clinical laboratory finding of DHF.

The major pathophysiological change that determines the severity of disease in DHF—and differentiates it from DF—is the leakage of plasma, as manifested by an elevated haematocrit (i.e. haemoconcentration), a serous effusion or hypoproteinaemia.

Children with DHF commonly present with a sudden rise in temperature
accompanied by facial flush and other non-specific constitutional symptoms
resembling DF, such as anorexia, vomiting, headache, and muscle or bone and joint pain. Some patients complain of sore throat, and an injected pharynx is frequently evident on examination, but rhinitis and cough are infrequent. Epigastric discomfort, tenderness at the right costal margin, and generalized abdominal pain are common. The temperature is usually high (.39°C) and remains so for 2–7 days. Occasionally, temperature may be as high as 40–41°C; febrile convulsions may occur, particularly in infants.

The most common haemorrhagic phenomenon is a:
· positive tourniquet test,
· easy bruising and bleeding at venepuncture sites.
· Present in most cases are discrete fine petechiae scattered on the extremities, axillae, face and soft palate, which are usually seen during the early febrile phase.
· Epistaxis and gingival bleeding occur infrequently;
mild gastrointestinal haemorrhage may be observed during the febrile period.
· The liver is usually palpable early in the febrile phase and varies in size from just palpable to 2–4 cm below the costal margin. Although liver size is not correlated with disease severity, an enlarged liver is observed more frequently in shock than in non-shock cases. The liver is tender, but jaundice is not usually observed.
· Splenomegaly is rarely observed in infants; however, the spleen may be prominent on X-ray examination.
· The critical stage of the disease course is reached at the end of the febrile phase. After 2–7 days of fever, a rapid fall in temperature is often accompanied by signs of circulatory disturbance of varying severity.
· The patient may sweat, be restless, have cool extremities and show some changes in pulse rate and blood pressure. In less severe cases, these changes are minimal and transient, reflecting a mild degree of plasma leakage. Many patients recover spontaneously, or after a short period of fluid and electrolyte therapy.
· In more severe cases, when plasma loss is critical, shock ensues and can progress rapidly to profound shock and death if not properly treated. The severity of the disease can be modified by early diagnosis and replacement of plasma loss.

Dengue shock syndrome (DSS)

The condition of patients who progress to shock suddenly deteriorates after a
fever of 2–7 days’ duration. This deterioration occurs at the time of, or shortly after, the fall in temperature—between the third and the seventh day of the disease. There are the typical signs of circulatory failure: the skin becomes cool, blotchy, and congested; circumoral cyanosis is frequently observed; the pulse becomes rapid. Patients may initially be lethargic, then become restless and rapidly enter a critical stage of shock. Acute abdominal pain is a frequent complaint shortly before the onset of shock.
DSS is usually characterized by a rapid, weak pulse with narrowing of the
pulse pressure (,20mmHg (2.7kPa), regardless of pressure levels, e.g. 100/
90mmHg (13.3/12.0kPa)) or hypotension with cold, clammy skin and restlessness.
Patients in shock are in danger of dying if appropriate treatment is not
promptly administered. Patients may pass into a stage of profound shock, with the blood pressure or pulse becoming imperceptible. However, most patients remain conscious almost to the terminal stage. The duration of shock is short: typically the patient dies within 12–24 hours, or recovers rapidly following appropriate volume-replacement therapy. Pleural effusion and ascites may be detected by physical examination or radiography. Uncorrected shock can give rise to a complicated course, with the development of metabolic acidosis, severe bleeding from the gastrointestinal tract and other organs, and a poor prognosis. Patients with intracranial haemorrhages may convulse and enter a coma. Encephalopathy, reported occasionally, can occur in association with metabolic and electrolyte disturbances or intracranial bleeding.
Convalescence in patients with corrected DSS is short and uneventful.
Even in cases of profound shock, once shock is overcome, surviving patients
recover within 2–3 days, although pleural effusion and ascites may still be
present. Good prognostic signs are adequate urine output and the return of
appetite.
Common findings during the convalescence of DHF patients are sinus
bradycardia or arrhythmia and the characteristic confluent petechial rash with small round areas of normal skin. Maculopapular or rubella-type rashes are less common in DHF than in DF and may be observed either early or late in the disease. The course of DHF is approximately 7–10 days. In general, there is no prolonged fatigue.

Laboratory findings

· Thrombocytopenia and haemoconcentration are constant findings in DHF. A drop in the platelet count to below 100000 per mm3 is usually found between the third and eighth day of illness, often before or simultaneous with changesin the haematocrit.
· A rise in the haematocrit level, indicating plasma leakage, is always present, even in non-shock cases, but is more pronounced in shock cases. Haemoconcentration with an increase in the haematocrit of 20% or more is considered to be definitive evidence of increased vascular permeability and plasma leakage. It should be noted that the haematocrit level may be affected either by early volume replacement or by bleeding. The time-course relationship between a drop in the platelet count and a rapid rise in the haematocrit appears to be unique for DHF; both changes occur before defervescence and before the onset of shock.
· In DHF, the white-blood-cell count may be variable at the onset of illness, ranging from leukopenia to mild leukocytosis, but a drop in the total whiteblood- cell count due to a reduction in the number of neutrophils is virtually always observed near the end of the febrile phase of illness.
· Relative lymphocytosis, with the presence of atypical lymphocytes, is a common finding before defervescence or shock.
· A transient mild albuminuria is sometimes observed,
· occult blood is often found in the stool.
· assays of coagulation or fibrinolytic factors show a reduction in fibrinogen, prothrombin, factor VIII, factor XII, and antithrombin III. A reduction in á-antiplasmin (á-plasmin inhibitor) has been noted in some cases. In severe cases with marked liver dysfunction, reductions are observed in the levels of the prothrombin factors that are vitamin-K dependent, such as factors V, VII, IX and X.
· Partial thromboplastin time and prothrombin time are prolonged in about one-half and one-third of DHF patients, respectively.
· Thrombin time is prolonged in severe cases. Platelet function has also been found to be impaired.
· Serum complement levels, particularly that of C3, are reduced.
· The other common findings are hypoproteinaemia (due to a loss of albumin), hyponatraemia, and elevated levels of serum aspartate aminotransferase. Metabolic acidosis may frequently be found in prolonged shock. Blood urea nitrogen is elevated at the terminal stage of shock.
· X-ray examination of the chest reveals pleural effusion, mostly on the right side, as a constant finding, and the extent of pleural effusion is correlated with the severity of disease. In shock, bilateral pleural effusion is a common finding.
Complications and unusual manifestations
As dengue infections have become more common, an increasing number
of cases of DF or DHF-like disease have been associated with unusual manifestations.
These include such central nervous system phenomena
· convulsions,
· spasticity,
· changes in consciousness and transient pareses.
· A subtle form of seizure is occasionally observed during the febrile phase in infants. This may be only a simple febrile convulsion, since the cerebrospinal fluid has been found to be normal in such cases.
· Water intoxication resulting from the excessive administration of hypotonic solution to treat DHF/DSS patients with hyponatraemia may lead to encephalopathy. Patients with encephalopathy as a complication of disseminated intravascular coagulation have also been reported.
· Intracranial bleeding may occur, and brain-stem herniation due to cerebral oedema has been observed.


Great care must be taken to prevent iatrogenic complications in the treatment of DHF/DSS, to recognize them quickly if they occur and not to mistake preventable and treatable iatrogenic complications for normal DHF/DSS findings.
Such complications include
· sepsis,
· pneumonia,
· wound infection and
· overhydration.

HOW TO PERFORM TOURNIQUE TEST
step 1- find systolic and diastolic bp of the patient
step2- inflate the bp cuff , to a midvalue between systolic and diastolic bp
step 3- keep as such for 5 minutes
step4- deflate and allow the skin to come back to the normal colour
step 5- count no: of petachiaes per inch square or per 6.25 cm square
POSITIVE TEST IS 20 OR MORE/ INCH SQUARE