A 28-year-old female, a known case of type 2 diabetes mellitus, hypothyroidism presented with high grade fever for 5 days, for which only symptomatic treatment taken. Went to primary clinic on day 6 – fever workup done – showed dengue NS1 and IgG positive. Investigations done outside revealed thrombocytopenia (Platelet:34000) and transaminitis (SGOT: 20, SGPT: 438) with total bilirubin: 1.68. No epigastric pain, vomiting, skin rashes, mucosal bleeding, syncope. On examination, afebrile, no skin rashes, tachycardic (PR 120bpm), BP: 140/90mmHg, RR: 22/min. Systemic examination showed no significant signs. Patient was admitted and started on IV fluid, liver protective drugs (SAM).
The same day evening she had 2 episodes of vomiting and BP: 100/70 mmHg; capillary refill was good. Blood investigations revealed further drop in platelets (22,000) and severe transaminitis (SGOT 7400; SGPT 1800). Patient was on IV fluids, in spite had a hypotension (BP:90/50mmHg), persistent tachycardia (130bpm) and tachypneic (40/min). Shifted to ICU and Started on non-invasive ventilation and inotropes. Blood gas analysis showed metabolic acidosis of pH7.1 with lactate 12. Repeat blood showed Hb of 12.7 (prev. 14.8) & Platelet: 10,000(prev. 22000). 1 unit SDP and PRBC transfusion and antifibrinolytic given.
Patient was kept on deteriorating and intubated in view of respiratory distress. Repeat blood gas analysis showed High anion gap metabolic acidosis [pH 6.9 & Lac-18; AG -22] and started on bicarbonate infusion and inotrope support increased to double strength.
Repeat liver function parameter showed a marked increase in transaminases (SGOT: 16,600, SGPT:2500) indicative of fulminant liver failure with coagulopathy [Prothrombin time (35) and INR (3.5)], for which N-Acetyl cysteine infusion given. The patient had nil urine output with gradual rise in creatinine, indicating acute renal shutdown, for which she started on continuous renal replacement therapy.
The general condition was deteriorating at a much rapid rate than improvement to symptomatic therapy. She had continuous ET bleed and circulatory collapse (BP: 90/60 on triple inotropes with maximal support). Repeat blood gas showed marked worsening of metabolic acidosis (pH 6.8) and developed bbradycardia with asystole.
Dengue is the most prevalent arthropod-borne viral disease worldwide, caused by flaviviruses (Dengue virus, subtypes 1-4). The principal vectors for all four viruses is the Aedes aegypti. With increasing spread of mosquitoes and travel by infected humans, large areas of the world have become vulnerable to infection. Infection with the dengue virus, may range from asymptomatic or undifferentiated febrile illness to fatal haemorrhagic fever.
Presence of warning signs warrants strict observation.
Severe plasma leakage is manifested by a rise or drop in haematocrit, fluid in the lungs or abdomen leading to respiratory distress, and dengue shock syndrome.
Individuals who are infected for the second time are at greater risk of developing severe dengue.
As in our case, patient had severe plasma leakage and marked elevation of transaminases and continuous mucosal bleeding.
Dengue Haemorrhagic Fever is a syndromic constellation of findings based on vascular instability and decreased vascular integrity. A direct or indirect assault on the microvasculature leads to increased permeability and (particularly when platelet function is decreased) to actual disruption and local haemorrhage (a positive tourniquet sign). Blood pressure is decreased, and in severe cases, shock supervenes. Haemorrhage occurs infrequently. In most patients, haemorrhage is an indication of widespread vascular damage rather than a life-threatening loss of blood volume.
Laboratory findings of dengue without/with warning signs include leukopenia, thrombocytopenia, and, in many cases, modest elevations of serum aminotransferase concentrations without hepatic synthetic dysfunction. The diagnosis is made by IgM ELISA or paired serology during recovery or by antigen-detection ELISA or RT-PCR during the acute phase.
Dengue haemorrhagic fever and dengue shock syndrome has higher mortality rates in all age groups. In our case, patient had no marked warning sign, but kept on deteriorating in the way that deterioration is much rapid rate than response to symptomatic therapy and had circulatory collapse and death within 36 hours of admission.
Dr Prabhakaran M DNB Internal Medicine Resident 1st year Kauvery Hospital, Chennai
Dr. S. Sivaram Kannan Clinical Lead & Chief Consultant Physician Kauvery Hospital, Chennai
