Original Article

Clinicolaboratory profile of expanded dengue

syndrome – Our experience in a teaching hospital
Bijaya Mohanty1, Ashok Sunder1, Saurabh Pathak2
Departments of 1Medicine and 2Gastroenterology, Tata Main Hospital, Jamshedpur, Jharkhand, India

A bstract
Introduction: Classic dengue fever presentation has expanded its horizon by involving various organ systems and is named as
expanded dengue syndrome. This changing presentation and rising burden across the globe may lead to delayed diagnosis and
under reporting of this syndrome. Aim of Study: To analyze clinicolaboratory profile of patients with expanded dengue syndrome.
Materials and Methods: About 520 cases of expanded dengue syndrome as per World Health Organization definition criteria 2012
were studied with their informed consent. Detailed history, thorough clinical examination, and relevant investigations were done.
Their clinical and laboratory parameters were analyzed. Standard treatment guidelines were followed in all cases. Observation: About
301 patients were male and 219 were female with male‑to‑female ratio of 3:2. Their age varied from 12 to 76 years with the average age
of 47.5 years. About 92% of cases presented with various gastro hepatic manifestations. The commonest gastrohepatic manifestation
was transaminitis (57.5%) that is asymptomatic elevation of liver enzymes followed by acalculous cholecystitis (21%) and acute
pancreatitis (13.9%). Twenty‑nine patients presented with various neurological manifestations. Three patients presented with acute
kidney injury and eight patients had coinfection with malaria. Fever with nausea and vomiting was the most common presentation.
About 15% of patients presented with bleeding manifestations. About 40.6% of patients presenting as abdominal manifestations had
platelet count <20,000/mm3 and needed platelet transfusion versus 9.8% with other system involvement (central nervous system,
cardiovascular system (CVS), renal). Hepatomegaly was the most common ultrasonography (USG) finding being present in 57.5% of
patients followed by acalculous cholecystitis in 21.3%. Total mortality was 1.9% in our series. We lost eight patients presenting with
neurological manifestations and two patients with coinfection with malaria. Conclusion: Atypical presentations should prompt us to
investigate for dengue especially during ongoing epidemics so that expanded dengue syndrome can be diagnosed and treated early.

Keywords: Acalculous cholecystitis, expanded dengue syndrome, transaminitis

Introduction clinicians but also a threat to the community at large. Dengue

virus is an arthropod borne virus of genus flavivirus belonging
Dengue fever is a mosquito‑borne viral disease, which has to family Flaviviridae. It is a single‑stranded RNA virus. There
reached alarming proportions in the past few years. It is are four genetically related but antigenically distinct DEN
endemic in over 100 countries.[1] About 40% of people all over serotypes (DENV‑1, DENV‑2, DENV‑3, DENV‑4) all of which
the world live in countries where dengue is endemic. Annually are prevalent in India.
390 million infections and 5,00,000 dengue hemorrhagic fever
cases have been identified. Dengue cases in India are also on The classic presentation of dengue fever has expanded its
a sharp rise over past few years to the tune of 28,292 cases in horizon by involving various organ systems. These system
2010 to 1,11,880 cases in 2016.[2] posing not only a challenge to specific presentations pose a diagnostic dilemma. Therefore,
World Health Organization (WHO), in 2012, incorporated a
Address for correspondence: Dr. Bijaya Mohanty, new terminology known as expanded dengue syndrome. In
Department of Medicine, Tata Main Hospital, expanded dengue syndrome, patient usually presents with atypical
Jamshedpur, Jharkhand, India.
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DOI: How to cite this article: Mohanty B, Sunder A, Pathak S. Clinicolaboratory

10.4103/jfmpc.jfmpc_12_19 profile of expanded dengue syndrome – Our experience in a teaching
hospital. J Family Med Prim Care 2019;8:1022-7.

© 2019 Journal of Family Medicine and Primary Care | Published by Wolters Kluwer ‑ Medknow 1022
 Mohanty, et al.: Expanded dengue syndrome – our experience

manifestations with various systemic involvement. Recognition

of features of expanded dengue syndrome (EDS) is very
important for targeting treatment option.

Aim of the study

We have undertaken this study with the aim to analyze the
clinicolaboratory profile of patients with expanded dengue
syndrome.

Materials and Methods

This is a hospital‑based prospective observational study. All Figure 1: Age and Sex variation
adults with clinical and laboratory parameters of serologically
confirmed cases of expanded dengue syndrome as per WHO Further system wise analysis was done. Out of 92% of
definition criteria were taken in to the study design with their cases presenting with various gastrointestinal and hepatic
informed consent and was conducted over a period of one year manifestations, 57.5% of the cases had features of asymptomatic
from April 2017 to March 2018. Cases with classical dengue fever, elevation of liver enzymes followed by 21.35% of cases who
dengue hemorrhagic fever, and dengue shock syndrome were
had features of acalculous cholecystitis. Acute pancreatitis
excluded from the study. Detailed history and thorough clinical
was detected in 12.88% of cases. Two patients had features
examination was done in all cases. Complete blood picture,
of subacute intestinal obstruction. They presented as acute
fasting blood sugar, serum creatinine, liver function tests, serum
abdomen. Initially, they were admitted in surgical ward and later
protein A/G ratio, viral markers (HIV, HBSAG, HCV), blood
transferred to medical ward after physicians’ review. All of them
for malaria parasite, chest radiograph, and ultrasonography of
improved with supportive care. Cerebral infarct and transverse
abdomen and pelvis were done in all cases. Other investigations,
myelitis were rare findings both contributing 0.19% each. Fever
such as computed tomography (CT) brain, electroencephalogram
with nausea and vomiting was the most common presentation
(EEG), magnetic resonance imaging (MRI) brain and spine,
followed by malaise and pain abdomen. About 9% of patients
lumbar puncture, and cerebrospinal fluid (CSF) examination were
presented with rashes; 15% of patients (n = 72) presented
done as and when indicated. Their age and sex distribution, signs
with bleeding manifestations; 36% of patients with abdominal
and symptoms, hematological parameters, clinical course of the
manifestations had petechiae followed by features of upper
illness, and outcome were analyzed in detail. They were treated
with intravenous fluids, antibiotics, blood and blood component gastrointestinal bleeding in 23% of cases [Figure 3].
therapy, and other supportive care as indicated. Statistical analysis
was performed using the SPSS software, Version 34. Total About 40.6% of patients presenting as abdominal manifestations
numbers and percentages were calculated for different categorical had platelet count <20,000/mm 3 in comparison to 9.8%
variables, such as clinical features and biochemical parameters. in patients who presented with other system involvement
(central nervous system [CNS], CVS, renal), which is statistically
significant (P‑value <0.0001). About 50.84% had their platelet
Observations count between 21,000 and 49,000/mm3. Only 8.56% of cases had
Overall, 1,493 cases of dengue fever were diagnosed as per WHO platelet count >50,000/mm3 [Figure 4]. About 57% of patients
criteria during the last academic year mentioned. About 520 cases who presented with abdominal symptoms along with features
were diagnosed to have expanded dengue syndrome and were of bleeding and low platelet count needed platelet transfusion.
taken into study design. About 301 patients were male and 219 Gastrointestinal involvement was correlated with platelet count
were female with male‑to‑female ratio of 3:2. Their age varied and Pearson correlation was found to be −0.3823 which is
from 12 to 76 years with the average age of 47.5 years. About 69% significant with a P value of <0.0001 and the 95% confidence
of patients belong to the age group of 31–60 years indicating that interval for r was −0.4534 to −0.3064.
mostly young and active people are getting the infection [Figure 1].
About 57.5% of cases of EDS showed elevation of transaminases.
Analysis of clinical manifestations revealed that most commonly aspartate aminotransferase (AST) peaked at day 4 of illness,
the gastrohepatic system was affected followed by CNS whereas alanine aminotransferase (ALT) peaked at day 6. After
involvement. In our series, we had 92% of cases of EDS who peaking at days 4 and 6, the AST and ALT levels gradually
presented with different gastrohepatic manifestation. About declined. The AST levels were much higher than ALT level.
5.5% cases presented with neurological symptoms. Three cases The mean AST levels on day 4 (mean 283.44, SD ± 20.1 IU)
had acute kidney injury who needed renal replacement therapy in were more than twofold when compared with the mean AST
the form of haemodialysis. Eight patients had coinfection with values (mean = 123.4, SD ± 41.8 IU). Hepatomegaly was
malaria and one patient had cardiovascular involvement in the the most common ultrasound finding in patients with EDS
form of sinus bradycardia [Figure 2]. being present in 299 (57.5%) patients followed by acalculous

Journal of Family Medicine and Primary Care 1023 Volume 8 : Issue 3 : March 2019
 Mohanty, et al.: Expanded dengue syndrome – our experience

have cerebral infarct after neuroimaging studies. Five patients had

meningitis all of whom improved with conservative management.
We had two patients who had features of hypokalemic palsy.
Their nerve conduction velocity and electromyography were
normal. They were treated with intravenous potassium chloride
infusion resulting in rapid improvement of their motor power.
Though spinal cord involvement in the form of acute transverse
myelitis is an uncommon manifestation we had one patient in
our series. His MRI spine showed segmental T2 hyperintensity
of the spinal cord from D4 to D6 level [Figures 5 and 6]
involving predominantly the central component. He was treated
Figure 2: Clinical manifestations
with injection methylprednisolone followed by adjuvant IVIG
2 g/kg (total 120 g) over 5 days and other supportive care along
with physiotherapy. He improved substantially after 4 months,
and after 7 months, he recovered completely.

Three cases of dengue presented with features of acute kidney

injury (AKI) were treated with renal replacement therapy and
improved. Eight cases had coinfection with malaria out of which
five cases developed multiorgan dysfunction. Four patients
survived and one with plasmodium falciparum expired after
a long stay of 42 days in critical care unit despite aggressive
management with ventilatory support, hemodialysis, blood
Figure 3: % Wise Bleeding Manifestation
and blood component therapy, and other supportive care.
Another patient with plasmodium vivax malaria and dengue
also succumbed the illness. He had G6PD deficiency too.
Total mortality was 1.9% in our series. We lost eight patients
presenting with neurological manifestations and two patients
with coinfection with malaria.

Discussion
Expanded dengue syndrome was coined by WHO in the year
2012 to describe cases which do not fall into either dengue
shock syndrome or dengue hemorrhagic fever. The atypical
manifestations noted in expanded dengue are multisystemic
and multifaceted with organ involvement, such as liver,
brain, heart, kidney, and CNS.[3] Patients with involvement of
Figure 4: Platelet count gastrointestinal and hepatic system may present with features
of asymptomatic elevation of liver enzymes, fulminant hepatic
failure, acute pancreatitis, acalculous cholecystitis, peritonitis,
cholecystitis, which was detected in 111 patients (21.3%). Serositis sub acute intestinal obstruction (SAIO), and rupture of spleen.
in the form of ascites and pleural effusion was also found in Lee et al. observed transaminitis in 30% of patients,[4] whereas
25.3% and 23.2% of cases, respectively. About 12.8% had we observed it in 57.5% of cases. Acalculous cholecystitis has
features of pancreatitis. Twenty‑nine cases presented with various been documented in many case reports. A study by Bhatty et al.
neurological manifestations. Fifteen patients had features of acute in 2009 reported 27.5% of cases as acalculous cholecystitis.[5] In
viral encephalitis. All of them presented with complains of fever our series, we had 21.3% cases of cholecystitis. Some studies
and altered sensorium. CT brain was done in all cases. Analysis also showed as high as 38% of cholecystitis in EDS.[6] These
of CSF was suggestive of viral encephalitis. They were treated patients had an increased levels of alkaline phosphatase,
aggressively. Ten patients recovered and five patients deteriorated thickened gallbladder wall, and pericholecystic fluid collection.
and developed multiorgan dysfunction, needed mechanical The pathogenesis of acute acalculous cholecystitis is still unclear.
ventilation, and other supportive care. Despite all measures Many factors are thought to contribute to liver dysfunction.
they succumbed to the illness. Intracranial bleed occurred in They are hypoxic injury due to decreased perfusion, direct
five patients. Three of them had massive intracranial bleed who damage by the virus, and immune‑mediated injury. Shaprio et al.
deteriorated rapidly and expired. Though bleeding complications in his studies showed that cholestasis, increased bile viscosity,
are well known in dengue fever, one patient was diagnosed to and infection are the probable causes.[7] However, the main

Journal of Family Medicine and Primary Care 1024 Volume 8 : Issue 3 : March 2019
 Mohanty, et al.: Expanded dengue syndrome – our experience

Figure 5: MRI Spine T2 Image showing Hyperintensity from D4-D6 level Figure 6: Transverse Section MRI Spine D4 level Showing Hyperintensity

cause which induces thickening of gall bladder wall is increased have encountered one patient who had bradycardia in expanded
vascular permeability, which causes plasma leakage and serous dengue. The pathophysiology of cardiac involvement in
effusion with high protein content mostly albumin. All patients dengue is variable. The favoured theory is that the virus cause
with acalculous cholecystitis recovered fully with conservative inflammation leading to cytokine storm causing loss of both
management. None of them required any surgical intervention structural and functional integrity. Localized insult due to minute
similar to other studies. Acute pancreatitis is an atypical and bleeding involving the SA node, AV node, or within its close
rare presentation.[8‑11] We had 67 cases of expanded dengue vicinity can also cause transient conduction abnormalities.[20,21]
presenting with features of acute pancreatitis, which was evident Neurological manifestations are more commonly observed and
by raised serum amylase and lipase and ultrasound findings. reported involving both central and peripheral nervous system.[22]
The exact pathogenesis of pancreatic involvement in dengue is Patient can present with features of encephalitis, meningitis,
not known. But it can be due to result of direct invasion by the stroke (both haemorrhagic and ischemic), hypokalemic paralysis,
virus itself causing inflammation and destruction of pancreatic encephalopathy, seizures, mono‑neuropathy, polyneuropathy,
acinar cells, an autoimmune response to pancreatic islet cells, and and Guillain‑Barre or Miller‑Fisher syndromes. Dengue virus
development of edema of the ampulla of Vater with obstruction infection involving spinal cord is extremely rare. Only few cases
to the outflow of pancreatic fluid.[12,13] Fortunately all our patients of transverse myelitis in patients with dengue fever have been
survived. We had two patients who presented with features of reported so far. We had 29 patients (5.5%) who had various
subacute intestinal obstruction. They improved with supportive neurological manifestations. Though bleeding complications
care. Only one case is documented so far in literature.[14] The are more common, we had one patient who had cerebral infarct.
exact pathophysiology of subacute intestinal obstruction is not We had five patients with meningitis and 15 with encephalitis.
known. Probably, it occurs due to edema of intestinal wall. These In these patients, there was CSF pleocytosis along with positive
patients presenting as intestinal obstruction usually get admitted enzyme linked immunosorbent assay (ELISA) for dengue.
in surgical wards. Same thing happened to our cases. They were We had one patient who was diagnosed as acute transverse
initially admitted in surgical ward and later transferred to medical myelitis following dengue infection. His MRI spine showed
side. Sometimes unnecessary surgery even takes place under segmental T2 hyperintensity of the spinal cord from D4 to D6
confusion as EDS may present in form of acute abdomen.[15] levels. There was no evidence of cord expansion or contrast
Even cases are reported where three uncommon presentations enhancement or involvement of the other segments of the
occurred concomitantly (acute acalculous cholecystitis, spinal cord. He was treated with injection methylprednisolone
acute pancreatitis, and pancytopenia) most likely due to followed by adjuvant IVIG 2 g/kg (total 120 g) over 5 days and
hemophagocytic syndrome.[16] other supportive care and improved. There are case reports
documenting transverse myelitis in dengue who were treated
Though sinus bradycardia is more common, patient may with steroid and immunoglobulins as we did.[23,24] The exact
present with features of myocarditis, pericarditis, acute pathogenesis of neurological manifestations of dengue viral
myocardial infarction, cardiomyopathy, sinoatrial (SA) node, infection is not known. However, there are several postulations.
atrio‑ventricular (AV) nodal block, and atrial fibrillation. Most important is either the neurotropic effect of the virus or
Dengue myocarditis incidence is low because it is asymptomatic the immune‑mediated injury or both. When the neurological
and diagnosis is easily missed. Almost all cases of dengue symptoms develop in peri‑infectious period, it is attributed to
myocarditis are self‑limiting and severe myocarditis leading direct viral invasion of the nervous tissue. Delayed appearance
to dilated cardiomyopathy is extremely rare.[17,18] Bradycardia of neurological disorders usually in postinfectious phase are
followed by complete heart block is also documented.[19] We considered to be due to immunologically mediated neural

Journal of Family Medicine and Primary Care 1025 Volume 8 : Issue 3 : March 2019
 Mohanty, et al.: Expanded dengue syndrome – our experience

injury.[25‑28] Acute hypokalemic quadriparesis is an uncommon physician to investigate for dengue specially during epidemics.
presentation of dengue fever, not yet widely recognized. Only A high degree of clinical suspicion is the key for early diagnosis
few cases are reported from various institutes worldwide. The and treatment. There is a rising tide of EDS. Our case series
mechanism of hypokalemia could be either due to redistribution may be the tip of the iceberg. Spreading increased awareness
of potassium in cells or transient renal tubular abnormalities among the community at large is the need of the hour to fight
leading to increased urinary potassium wasting. We had two this syndrome which mimic a myriad of clinical conditions.
patients with hypokalemic quadriparesis who improved after
potassium supplementation similar to other case reports.[28] Financial support and sponsorship
Patients with neurological manifestations especially encephalitis Nil.
have high mortality as shown in recent studies which is similar
to our observation too.[29] Conflicts of interest
There are no conflicts of interest.
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