Dengue Shock Syndrome with Fulminant Liver Failure

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.

DISCUSSION

Introduction:

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.

Phases of dengue fever:

• Febrile phase (2-5 days)
• Critical phase (1-2 days) – characterized by plasma leakage, and
• Recovery phase (1-2 days)

Warning signs of Dengue fever:

• Abdominal pain or tenderness
• Persistent vomiting
• Clinical fluid accumulation
• Mucosal bleeding
• Lethargy
• Restlessness
• Liver enlargement greater than 2 cm, and
• An increase in haematocrit concurrent with rapid decrease in platelet count.

Presence of warning signs warrants strict observation.

Classification of Dengue fever:

• Non-severe dengue fever: sudden onset of high fever associated with rash, severe muscle, and joint pains, and any of the warning signs. These symptoms gave rise to term “break-bone fever.”
• Severe dengue haemorrhagic fever (previously dengue haemorrhagic fever and dengue shock syndrome): Marked by significant plasma leakage, hemorrhaging, and organ engagement exhibited as elevated liver enzyme levels, impaired cognitive function, and myocarditis. A positive tourniquet test signifies a severe form of the illness.

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.

Diagnosis:

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.

Prognosis:

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 1^st year
Kauvery Hospital, Chennai

Dr. S. Sivaram Kannan
Clinical Lead & Chief Consultant Physician
Kauvery Hospital, Chennai