Mr ZK, a 56-year-old male with underlying heart failure and hypertension referred to the emergency department of a district hospital in the northern Selangor state of Malaysia complaining of fever and generalised point pain for 4-days. This is a district hospital with 150 beds, run mainly by medical officers with occasional outpatient visits by specialists. It has four wards, one combined general medical and surgical each for males, females and paediatric age group, one obstetrics and gynaecology ward and one emergency ward. Due to non-availability of 24-hour specialist services at the hospital, serious and life-threatening cases, who may need urgent surgery or ventilation are referred to the nearest tertiary hospital located about 60 km away. Other than fever and arthralgia, Mr ZK also had vomiting and diarrhoea for two days associated with loss of appetite. There was no shortness of breath, abdominal pain, decrease in urine output or bleeding tendencies. Two days earlier, he had sought treatment at a nearby general practitioner clinic yet his symptoms remained unresolved. His last paracetamol intake was 24 hours ago.
On physical examination, Mr ZK was alert and conscious. His vital signs were stable, including a blood pressure of 140/90 mmHg, pulse rate 96 beats per minute, temperature of 37.1°C, and respiratory rate of 16 breaths per minute. His body mass index was 32.3 kg/m
2, placing him into the category of obesity. The measurement of the vital signs, weight, and height were done with regular calibrated medical equipment, including a sphygmomanometer, mercury thermometer, weighing machine, and stadiometer. His hydration and perfusion status was otherwise good. On cardiovascular examination, the jugular venous pressure was normal at 4 cmH 2O (normal level taken ≤ 4 cm) and the apex beat was slightly displaced at the fifth intercostal space 1 cm lateral to the left midclavicular line. There was bilateral pedal oedema up to the mid-shin. The respiratory examination showed bilateral basal crepitation. Abdominal and back examination did not show any ascites or sacral oedema, respectively.
Investigations showed a haemoglobin of 14 g/L, haematocrit of 45%, reduced white blood cell count of 2.7 × 10
9/L, and a low platelet of 75 × 10 9/L, based on investigations done on a venous blood sample at the validated full blood count machine in the same hospital. A raised haematocrit usually indicates plasma leakage in a patient with dengue. In patients with previously unknown baseline haematocrit level, haematocrit level of ≥ 46% and ≥ 42% in Malaysian males below and above the age of 60 years old usually indicates raised haematocrit compared to ≥ 40% in Malaysian females ( 2). According to the world health organization, significant thrombocytopenia in dengue fever is < 100 × 10 9/L, as thrombocytopenia can also be caused by drug intake or other viral infections ( 2). Other blood tests including renal profile, liver function test, coagulation profile, and random blood sugar, were unremarkable except for a mild increase in liver transaminases. Dengue serology for immunoglobulin M antibodies was also ordered, which turned out to be positive.
Classifying this case as dengue fever in the defervescence phase and acknowledging the chronic medical problems that this patient was having, including hypertension and chronic heart failure and the fact that he was obese (which are all markers of severe dengue and hence higher risk of dengue-related fatality), he was admitted to the ward. In the ward, his oral furosemide of 40 mg once a day was converted to the intravenous form of the same dose. Strict input and output chart was started together with daily body weight monitoring.
Initially, Mr ZK was started on 2 pints of normal saline daily, with adjustment to be made according to his urinary output and body weight. If urinary output remained above 500 mLs and weight gain was less than 2 kg over 2 days, this fluid regimen was continued. There was no change in this fluid regimen as Mr ZK was passing about 600 to 700 mLs of urine per day and his weight did not increase beyond 2 kg in addition to absence of acute heart failure symptoms and signs, except bilateral pedal oedema up to mid-shin and bilateral basal lung crepitation.
His full blood count also showed improvement in his platelet count (75 to 70 to 72 to 80 × 10
9/L) and haematocrit (45% to 44% to 42% to 41%). White blood cell count normalised to 4.2 × 10 9/L and haemoglobin remained within the normal range. These findings are summarised in Table 1.
Table 1. Summary of Full Blood Count Parameters for Mr ZK
Day Parameters White Blood Cell CounT, × 10 9/L Haemoglobin, g/L Haematocrit, % Platelets, × 10 9/L 1 (admission) 2.7 14.2 45 75 2 2.6 14.1 44 70 3 3.4 13.9 42 72 4 (discharge) 4.2 14.0 41 80
Table 2. Management of Fluid Overload in Patients with Dengue Fever
Haemodynamic Status Presence of Shock Haematocrit Management Unstable Yes High Colloid fluid bolus 10 mL/kg over an hour. Intravenous furosemide 10 - 20 mg bolus at 30 minutes of starting the colloid bolus and repeated if necessary Unstable Yes Low or normal (possible massive internal bleeding) Urgent blood transfusion. While awaiting for blood to arrive, 500 mL of colloid fluid bolus can be administered Stable No Normal or low Advise for fluid restriction with careful regular monitoring. Intravenous frusemide 10 - 20 mg can be given in the presence of acute pulmonary oedema and repeated every 30 minutes as necessary Stable No High Advise for fluid restriction with careful regular monitoring. In patents with fluid overload as evidenced as massive pleural effusion or gross ascites and poor peripheral circulation, therapeutic aspiration is advised.
With improvements in his oral intake and blood parameters, including cessation of vomiting and diarrhoea and presence of stable vital signs, he was discharged with his old medications and advised to take between 1 and 1.5 litres of fluid daily. He was seen one week later, when repeat platelet count showed a marked improvement to 272 × 10
The study of this case indicated that it is possible to manage the co-morbidity of heart failure and dengue fever by paying attention to fluid balance and clinical parameters, and also had lessons on maintaining a good fluid balance. In the literature, there is a significant absence of reporting of such cases i.e. managing dengue fever in the presence of heart failure. Weak points were that perhaps a specialist advice should have been sought which wasn’t, as heart failure cases can deteriorate very fast, especially when decompensation occurs. Furthermore, if the patient was admitted to a tertiary hospital with more manpower and availability of ventilators, it is unclear whether invasive or non-invasive ventilation would have been a better option.