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Table of Contents
CASE REPORT
Year : 2020  |  Volume : 8  |  Issue : 4  |  Page : 194-198

A case series of atypical manifestations of dengue


Department of General Medicine, MVJ Medical College and Research Hospital, Bengaluru, Karnataka, India

Date of Submission05-Nov-2019
Date of Decision24-Dec-2019
Date of Acceptance27-Dec-2019
Date of Web Publication23-Oct-2020

Correspondence Address:
Dr. C H. Monica Lakshmi Priyanka
MVJ Medical College and Research Hospital, Hoskote, Bengaluru - 562 114, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AJIM.AJIM_71_19

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  Abstract 


Dengue fever is an arthropod-borne viral illness caused by Flavivirus and transmitted by Aedes aegypti mosquito. With rising burden of disease, atypical manifestations have increased. In our case series, we report five cases of serologically proven dengue-positive patients (by immunochromatographic dengue card test) with atypical manifestations. The first two patients presented with dengue encephalitis and the next two patients presented with viral pneumonia. The second, fourth, and fifth cases were dengue in cirrhotic patients leading to decompensated liver disease. The fourth case succumbed to death due to refractory shock. We should have a high index of suspicion and knowledge to detect atypical manifestations of dengue fever as they are more fatal and are increasing in incidence. In preexisting liver disease, chances of bleeding are high even though platelet counts are not very low. Only appropriate timely intervention can prevent morbidity and mortality.

Keywords: Dengue, dengue encephalitis, dengue in cirrhotic


How to cite this article:
Priyanka C H, Bindu B H, Nivea B, Jacob M J. A case series of atypical manifestations of dengue. APIK J Int Med 2020;8:194-8

How to cite this URL:
Priyanka C H, Bindu B H, Nivea B, Jacob M J. A case series of atypical manifestations of dengue. APIK J Int Med [serial online] 2020 [cited 2020 Nov 30];8:194-8. Available from: https://www.ajim.in/text.asp?2020/8/4/194/298942




  Introduction Top


Dengue fever is an arthropod-borne viral illness caused by RNA viruses of Flaviviridae and transmitted by Aedes aegypti mosquito. The incubation period is 2–7 days. Patients can be asymptomatic to symptomatic. Symptoms in the initial febrile phase which lasts for 3–7 days include fever, retro-orbital headache, arthralgia, and rash. Next is critical phase which lasts for 24–48 h, where there is extravasation of plasma into third spaces causing polyserositis, hypovolemia, bleeding manifestations, and multiorgan involvement. This phase has to be treated aggressively with intravenous (IV) fluids. Following this phase is convalescent phase or resolution phase in which the fluid is reabsorbed back into the intravascular compartment. This phase lasts for 2–5 days.[1]

The virus has four serotypes. Infection with one serotype gives lifelong immunity to the same serotype whereas only temporary immunity to other serotypes. When infection is caused by multiple serotypes or is associated with secondary infections, manifestation is much severe.[2],[3],[4] With rising burden of disease, atypical manifestations have increased.

In this case series, we present the serologically proven (by immunochromatographic dengue card test) dengue patients with atypical manifestations, as they have a good learning point to recognize atypical cases early and prevent morbidity and mortality.


  Case Report Top


Case 1

A 60-year-old male presented with a 4-day history of fever associated with headache and one episode of vomiting. The patient started to talk irrelevantly and showed violent behavior on the 4th day for which he was brought to our hospital. There was no history of seizures, rash, joint pains, or bleeding manifestations. There was no history of alcohol intake. On examination, the patient was in altered sensorium. Pulse rate was 66/min, blood pressure (BP) – 160/70 mmHg, oxygen saturation (SPO2) – 99% at room air, and temperature – 98.6 F. There were no signs of meningeal irritation or focal neurological deficits. Other system examinations were normal. Ocular fundoscopy was normal. Noncontrast computed tomography (NCCT) brain showed only age-related cerebral atrophic changes [Figure 1]. Hence, cerebrospinal fluid (CSF) analysis was done which showed increased protein of 55 mg/dl, normal sugars of 115 mg/dl, and 110 cells/μl showing lymphocyte predominance which was suggestive of viral etiology. Adenosine deaminase (ADA) levels were normal, and CSF culture showed no growth. Complete hemogram showed white blood cells (WBCs) of 14,400 cells/mm3 and platelets of 3.45 lakhs/mm3. Renal and liver functions and serum electrolytes were fairly normal. He was also detected positive for dengue IgM antibody. Peripheral smear for malarial parasite was negative and Weil-Felix test was negative. The patient responded well without antitubercular therapy. Hence, the diagnosis of dengue encephalitis has been made as other causes of encephalitis were ruled out, even though CSF for dengue virus isolation or antibodies could not be done due to financial constraints.
Figure 1: Noncontrast computed tomography brain – age-related cerebral atrophy

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The patient was managed conservatively with IV fluids and other supportive treatments. The patient's sensorium improved but mild headache persisted. After 2 days, he again developed altered sensorium. Repeat fundus examination showed blurring of bilateral disc margin. Hence, he was treated with IV mannitol and injection dexamethasone after which headache subsided. The patient was discharged after 10 days of treatment with complete recovery.

Case 2

A 49-year-old diabetic male presented with fever and generalized weakness of 4-day duration and a 1-day history of irritable behavior. There was no history of vomiting, rash, and seizures. There was no history of alcohol consumption or altered sleep pattern. Appetite was good, and the patient was regular at work before presentation at hospital. On examination, the patient was in altered sensorium. Pulse rate was 100/min, BP – 140/70 mmHg, temperature – 99.6 F, SPO2 – 99% at room air, and random blood sugar – 270 mg/dl. On neurological examination, there were no signs of meningeal irritation. On cardiac examination, there was a pansystolic murmur in the tricuspid area. The abdomen was distended, nontender and free fluid was present. The respiratory examination was normal. NCCT brain and CSF analysis done were normal. CSF ADA was normal. The patient was tested positive for dengue IgM antibody. Peripheral smear for malarial parasite was negative and Weil-Felix test was negative. CSF for dengue virus isolation and antibodies could not be done due to financial constraints. Complete hemogram showed hemoglobin (Hb) – 9.5 g/dl, WBC count – 5520 cells/mm3, and platelets – one lakh cells/mm3. Liver function tests showed total bilirubin of 4.2 mg/dl, serum glutamic-oxaloacetic transaminase (SGOT) – 71 IU/L, Serum glutamic-pyruvic transaminase (SGPT) – 62 IU/L, and alkaline phosphatase (ALP) – 154 IU/L. Prothrombin time (PT) was 15.1, international normalized ratio (INR) – 1.11, and activated partial thromboplastin time (APTT) – 34.0. Ultrasound abdomen showed cirrhosis of the liver, gross splenomegaly, and ascites picture suggestive of cirrhosis with portal hypertension. Echocardiography was normal. Hence, the diagnosis of dengue encephalitis in a patient with already existing liver cirrhosis was made. As serum bilirubin and liver enzyme raise is mild, encephalopathy cannot be explained as hepatic encephalopathy. However, any infection can precipitate hepatic encephalopathy, and to exclude it, serum ammonia levels could have been done. Again, it could not be done due to financial constraints. The patient was managed conservatively with IV antibiotics, IV fluids, insulin, syrup lactulose, and other supportive treatments. Platelet counts dropped up to 80,000 cells/mm3 in the successive days and were monitored daily. The patient had one episode of small-volume hematemesis and hence transfused with two packs of whole blood. The patient recovered completely with the above treatment. There was no further hematemesis or bleeding manifestations. Platelet count after 10 days at the time of discharge improved to 1.2 lakhs/mm3.

Case 3

A 70-year-old female patient, with no known comorbidities, presented with a history of abdominal distension for 1 week, constipation for 6 days, fever, and breathlessness at rest for 4 days. Fever was continuous, moderate grade, associated with chills, myalgia, and joint pains. On examination, the patient was conscious, cooperative, and well oriented to time, place, and person. Pulse rate was 102/min, BP – 130/70 mmHg, respiratory rate – 18 cpm, temperature – 98 F, and SPO2 – 85% at room air. On examination, the abdomen was soft, nontender, and distended with free fluid and bowel sounds were normal. Bilateral coarse crepitations (right > left) were present on chest auscultation. The rest of the systems were within normal limits. Complete hemogram done showed WBC of 13,800 cells/mm3 and platelets of 44,000 cells/mm3. Liver and kidney function tests were fairly normal. Ultrasound abdomen showed right moderate and left mild hydronephrosis and minimal ascites. Chest X-ray revealed diffuse infiltrates bilaterally suggestive of viral pneumonia [Figure 2]. The patient was detected positive for dengue IgM antibody. Arterial blood gas analysis (ABG) showed pH – 7.23, PO2 – 50 mmHg, PCO2 – 47 mmHg, and HCO3 – 21 mmol/l suggestive of respiratory acidosis.
Figure 2: Chest X-ray – Diffuse infiltrates bilaterally suggestive of viral pneumonia

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The patient was treated with oxygen, antibiotics, oseltamivir, nebulization, laxatives, IV fluids, and other supportive treatments. Platelet count has been monitored regularly. The patient had improved gradually and was discharged after 8 days of hospital stay. Platelet count at discharge increased to 1.6 lakhs/mm3.

Case 4

A 50-year-old female patient, hypertensive and diabetic, presented with fever and cough with expectoration of 1-week duration, breathing difficulty for 1 week which increased for 1 day, and anuria for 1 day. There was no history of rash, joint pains, pain abdomen, and bleeding manifestations. There was no history of chest pain, palpitations, and paroxysmal nocturnal dyspnea. The patient is an alcoholic and known case of chronic liver disease, has been taking treatment for several years, and was admitted thrice for the same. The patient was conscious, oriented, but very irritable. Pulse rate was 124/min, BP – 100/60 mmHg, respiratory rate – 38 cpm, temperature – 97.6 F, and SPO2 – 65% with room air and 97% with 4 l O2. Pallor, Grade 2 clubbing, and mild pedal edema were present. The patient was conscious, oriented, but very irritable. There were no focal neurological deficits. Respiratory examination revealed coarse crepitations in bilateral mammary, infrascapular, interscapular, and infra-axillary areas. The abdomen was distended, soft, and nontender with free fluid; there was no organomegaly, and bowel sounds were heard. The cardiac examination was normal. Complete hemogram showed Hb of 9.2 g/dl, WBC – 6720 cells/mm3, and platelets – 1.2 lakhs/mm3. Renal functions were deranged with urea of 156 mg/dl and creatinine of 3.1 mg/dl. The total bilirubin was 1 mg/dl, SGOT – 101 IU/L, SGPT – 81 IU/L, ALP – 102 IU/L, and albumin – 2.2 g/dl. PT was 20, INR – 1.5, and APTT – 40. Chest X-ray done showed bilateral diffuse patchy opacities suggestive of viral pneumonia [Figure 3]. ABG showed pH of 7.21, PO2 – 43 mmHg, PCO2 – 58 mmHg, and HCO3 – 15 mmol/l suggestive of mixed acid-base disorder. The patient was detected positive for dengue IgM antibody.
Figure 3: Chest X-ray – Bilateral diffuse patchy opacities suggestive of viral pneumonia

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The patient has been intubated and put on mechanical ventilator in view of acute respiratory distress syndrome (ARDS). Antihypertensives withheld. The patient developed hypotension on the 2nd day, and hence, inotropes were started. IV fluids, antibiotics, lactulose, insulin, and other supportive treatments were given. Five Pints of Fresh Frozen Plasma transfused as coagulation profile was deranged. There was an initial improvement in BP, urine output, and renal functions on day 2 but worsened again. Despite all necessary measures, the patient condition further deteriorated and succumbed to death due to dengue shock syndrome and multiorgan dysfunction syndrome (MODS).

Case 5

A 55-year-old male patient presented with a history of fever of 1 week, abdominal distension, and bilateral lower limb swelling which increased after the onset of fever. The patient is an alcoholic and known case of liver cirrhosis. The patient was conscious, cooperative, and well oriented. Pulse rate was 112 bpm, BP – 100/60 mmHg, temperature – 99 F, and respiratory rate – 16 cpm. Bilateral pitting pedal edema was present. The abdomen was distended with free fluid. There were no flapping tremors. The rest of the systemic examination was normal. Complete hemogram showed Hb – 7.3 g/dl, WBC – 2600 cells/mm3, and platelets – 40,000/mm3. Total bilirubin was 12.9 mg/dl, direct bilirubin – 4.2 mg/dl, indirect bilirubin – 8.7 mg/dl, SGOT – 78 IU/L, SGPT – 32 IU/L, ALP – 73 IU/L, Serum Total Protein – 6.4 g/dl, and Serum Albumin – 2.4 g/dl. PT was 19.5, INR – 1.61, and APTT – 46.7. The patient was detected positive for dengue IgM antibody. Ultrasound abdomen showed liver cirrhosis with portal hypertension.

The patient has been treated for the liver condition as well as dengue fever with diuretics, rifaximin, laxatives, and Vitamin K. The use of nonsteroidal anti-inflammatory drugs was limited owing to the liver condition. The patient developed bleeding manifestations in the due course. Serial platelet and coagulation profile monitoring was done. Eight Pints of FFP was given. However, there was only marginal improvement. Abdominal paracentesis could not be done due to deranged coagulation parameters. The patient was hence referred to a gastroenterologist for further management.


  Discussion Top


With an average incubation period of 4–6 days, dengue fever presents with diffuse flushing over the body. On the 3rd day of illness, it evolves into maculopapular rash. Subsequently, rash fades and petechiae appear at defervescence. Just before, the defervescence is the critical phase when plasma leak happens along with thrombocytopenia and leukopenia. When not monitored or treated properly, it can progress to shock.

As per the WHO guidelines for dengue fever, unusual or atypical manifestations are also termed as “expanded dengue syndrome.”[4] These could be complications of profound shock or coinfections or underlying host conditions or diseases.

Atypical manifestations

Various atypical manifestations of dengue include hepatitis causing transaminitis, fulminant hepatic failure, acalculous cholecystitis, renal failure, febrile diarrhea, myocarditis, conduction abnormalities in heart, pericarditis, and ARDS. Rarely, acute pancreatitis can also happen.

Until recently, dengue virus was considered as a nonneurotropic virus.[5] However, neurological manifestations have been increasingly reported in recent years[6],[7],[8],[9],[10] such as encephalopathy or encephalitis and aseptic meningitis. Neurological manifestations can also include seizures, intracranial hemorrhage, and neuropathies. In our case series, two patients presented with encephalitis with no complication of seizures. The central nervous system manifestations can be attributed to three factors: (a) direct neurotropic effect of the virus, (b) secondary to systemic manifestation, and (c) postinfectious sequelae including immune-mediated reactions.[10],[11]

Abdominal symptoms are the most important and most common in dengue fever. These are warning signs before worsening to severe dengue. Hepatitis is due to direct cytopathic effect of virus on liver cells. Fulminant hepatic failure is secondary to shock and disseminated intravascular coagulation in severe illness. Acalculous cholecystitis presents with gallbladder mucosal edema and pericholecystic fluid without any gallstone (in ultrasound) and is secondary to plasma vascular leakage. Rarely, acute pancreatitis can occur which is due to direct cytopathic effect of virus or autoimmune response by molecular mimicry.

In the above cases, transaminitis was present in four cases; two cases had ultrasound evidence of dengue-like illness. Three patients had liver cirrhosis which progressed to decompensated liver disease. One of these patients succumbed to death due to refractory shock.

Acute lung injury or ARDS is one of the most dreaded complications of dengue hemorrhagic fever. They occur secondary to increase alveolar–capillary membrane permeability causing interstitial and alveolar edema. Here, the third and fourth cases presented with viral pneumonia of which one succumbed to death.

Renal failure is mainly due to shock-induced acute tubular necrosis. It could also be due to MODS and rhabdomyolysis. Of the above cases, the fourth case had developed renal failure.

Cardiac manifestations such as conduction blocks, atrial fibrillation, and ectopic ventricular beats are due to myocarditis. There were no cardiac manifestations in the above five cases.

All the above complications can lead to high mortality if not recognized and treated well in time. The fourth case had liver disease complicated with dengue and MODS. Thus, multiorgan involvement in already unhealthy patients could have led to death of the patient.

Learning points: symptoms such as headache, vomiting, and altered sensorium are warning signs, and high vigilance is required. Cases of Dengue with preexisting co-morbidities such as cirrhosis should be carefully watched. One should watch for bleeding in the presence of liver disease even though platelets are not very low (second case).


  Conclusion Top


Dengue can have atypical presentations such as encephalitis, ARDS, and renal failure. In preexisting liver disease, chances of bleeding are high even though platelet counts are not very low. We should have a high index of suspicion and knowledge to detect atypical manifestations of dengue fever as they are more fatal and are increasing in incidence. Only appropriate timely intervention can prevent morbidity and mortality.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Kalayanarooj S, Nimmannitya S. Guidelines for Dengue Hemorrhagic Fever Case Management. Bangkok: Bangkok Medical Publisher; 2004.  Back to cited text no. 1
    
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Bhoi SK, Naik S, Kumar S, Phadke RV, Kalita J, Misra UK. Cranial imaging findings in dengue virus infection. J Neurol Sci 2014;342:36-41.  Back to cited text no. 5
    
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Li GH, Ning ZJ, Liu YM, Li XH. Neurological manifestations of dengue infection. Front Cell Infect Microbiol 2017;7:449.  Back to cited text no. 6
    
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Ruikar D, Jayalakshmi S, Surath M. Neurological manifestations of acute dengue virus infection: A study from tropical country- India (I4-5D). Neurology 2015;84:14D-5D.  Back to cited text no. 7
    
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Misra UK, Kalita J, Syam UK, Dhole TN. Neurological manifestations of dengue virus infection. J Neurol Sci 2006;244:117-22.  Back to cited text no. 8
    
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Pal S, Sen K, Biswas NM, Ghosal A, Rousan Jaman SK, Yashavantha Kumar KY. Clinico-radiological profile and outcome of dengue patients with central nervous system manifestations: A case series in an Eastern India tertiary care hospital. J Neurosci Rural Pract 2016;7:114-24.  Back to cited text no. 9
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Verma R, Sahu R, Holla V. Neurological manifestations of dengue infection: A review. J Neurol Sci 2014;346:26-34.  Back to cited text no. 10
    
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