Figure 1: Chest X-ray dated 17th October showing bilateral
pleural effusion
Upon receiving the patient in the Emergency Department, pulse and blood
pressure were recorded as 63 beats/minute and 94/50 mmHg, and he was
physically assaulting family and staff members alike along with
displaying resistance to therapeutic care by removing cannulas and
nasogastric tubes; he also showed impedance to taking medicine. On
evaluation by the Psychiatry Department, he was under the impression of
delirium. The Laboratory investigations conducted are reported in
Table 1,
which evidently reports deranged Liver Function Test values. The patient
was injected with one liter of Ringer’s Lactate to stabilize his vitals
and was then advised admission to the Medical HDU.
The patient was received in Medical HDU in a drowsy state (not oriented)
and on repeated examination, vitals were as noted: Pulse- 66
beats/minute, Blood Pressure- 130/80 mmHg, and respiratory rate- 24
breaths/minute. The abdomen was examined to be flat with the umbilicus
centrally placed and inverted, with the lower edge of the liver palpable
1 cm below the costal margin with moderate tenderness in right
hypochondrium, no splenomegaly appreciated ,signs of free fluid present
with positive shifting dullness Pupils were found to be equally reactive
to light bilaterally .
The patient was shifted to Medical ICU on 20th October 2022 with the
Laboratory findings described in
Table 1 and
being treated along the lines of Fulminant Liver Failure. The
progressive fluctuations in hemoglobin levels, Total Leukocyte count,
Platelets count, and electrolyte levels since before and during
admission in the ICU are tabulated in
Table 1.
The patient was subjected to the treatment regimen, which included
Meropenem 1 gm IV x TDS, Risek 40 mg IV x OD, N-acetylcysteine 150 mg/kg
in 5 divided doses Loading dose of 150mg/kg in 100ml 5% dextrose water
over 15 minutes with the maintenance dose of 12.5 mg/kg/hour over 4
hours and third dose of 6.25 mg/kg/hour over 16 hours, Mannitol 200 ml
IV stat then 100 ml IV x OD (3 days) and syrup Duphalac 30 ml BD
The patient tested positive for Dengue IgM Antibody and an Ultrasound of
the whole abdomen was concurrently performed on 22nd October, with the
findings as follows-
· Liver - Normal in size measuring 15.1 cm with irregular outline and
decreased parenchymal echogenicity. The portal vein was 1.0 cm, while
the intrahepatic duct and vessels showed no abnormality. No focal mass
was visualized.
· Gall-bladder - A thick, hypoechoic wall measuring 1.0 cm was
conceived. There were no mass or calculi apprehended, and the common
bile duct was found to be 0.4 cm in diameter. The findings were denoted
as acute acalculous cholecystitis.
· No abnormal finding was reported in the pancreas and spleen.
· Kidneys - Bilaterally normal in size, shape, and position.
Bilaterally, renal parenchymal changes were observed.
· General - Gross ascites was evident, bilateral gross pleural effusion
secondary to lung collapse.
The patient became tachypnic and tachycardic with drop in GCS due to
which patient was electively intubated on 21st October 2022. The patient
gradually developed scrotal swelling which was evaluated by the Urology
Department on 26th October 2022. The department commented on the patient
having generalized body swelling which was predisposed to scrotal
swelling. The patient was currently on a mechanical ventilator and
required only scrotal support and elevation for relief. However, he
developed an abnormal breathing rhythm which was found secondary to
blockage of the endotracheal tube with blood clots signifying massive
internal hemorrhage. 4 packs of Fresh Frozen Plasma (FFP), 6 packs of
platelets, and 1 bag of Packed Cell Volume (PCV) was transfused to
combat the deteriorating hemodynamics of the patient.
The patient succumbed to the disease at 10:18 A.M. on 27th October
secondary to cardiopulmonary arrest as a complication of acute and
subacute liver failure.
Discussion
Dengue is typically reported to the clinical setting with a history of
high grade fever, and drastically depleting platelets. Plasma leakage is
also a usual finding and its progress manifests as either compensated,
or uncompensated shock. The shock syndrome may confer lethality by
causing multi-organ failure or death. The term ‘Expanded Dengue
Syndrome’ amalgamates the findings exacerbating from the usual clinical
picture and manifesting as an unusual
presentation [9].
Liver involvement is prevalent among people infected with Dengue virus,
most commonly founded in the form of elevated transaminase levels.
Escalating levels of serum glutamic-oxaloacetic transaminase and serum
glutamic-pyruvic transaminase are in corollary to disease severity and
are indirectly proportional to platelet
counts [10].
Concomitant complains of abdominal pain, anorexia, nausea and vomiting
are strong indicators of liver involvement in a diagnosed dengue
patient [11].
A myriad of factors contributes towards liver involvement constituting
direct damage and loss of hepatocytes, and indirect damage mediated by
the host immune system which jeopardizes vascular and circulatory
integrity and may also exhibit metabolic dysfunction such as acidosis
and
hypoxia [12].
Certain chemokines such as Interleukin 17 and Interleukin 10 (IL-17,
IL-10) are also implicated in cases of severe hepatic involvement in the
absence of prominent fluid leakage and endothelial damage, where immune
mediators are expected to be
involved [13].
According to a study conducted by Jayaratne et al., the presentation of
abdominal pain, vomiting, clinical fluid accumulation, and mucosal
bleeding was persistently high in Dengue patients who developed severe
disease. Laboratory parameters including a mean Platelet count
< 20,000/mm, Aspartate Transaminase Levels > 45
IU, and lymphocytes < 1500 were significantly associated with
severe
disease [14].
Conclusions
Our case emphasizes the lethality of Dengue fever and its complications
when the case is bought into clinical attention once hepatic
encephalopathy has developed. Infection by Dengue Virus was proven
practically days after signs and symptoms developed which was
significantly contributory factor towards the poor outcome in this
patient. Fulminant Hepatic Failure ensued with significant capillary
leak and overt bleeding which manifested acutely before the patient
expired.
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