Ccs agustus '07.indd

Crit Care & Shock (2007) 10 : 111-114 Signifi cantly Raised Brain Natriuretic Peptide in a Young Patient
with Dengue Fever without Heart and Renal Failure
Ashish A. Sule, Dessmon YH Tai, Koh N Yue, Veerendra Chadachan, Kenneth Ng
Abstract
Objective: This is the fi rst case report of association
of heart failure. There was no renal impairment
of raised brain natriuretic peptide (BNP) in
or systemic infl ammatory response syndrome. A
patients with dengue fever (DF). BNP is raised in
transthoracic 2-dimensional echocardiography was
patients with heart failure. It can also be elevated
in renal failure and subarachnoid haemorrhage in
the absence of heart failure. Raised BNP has never
Treatment: Patient was treated with intravenous
been described in patients with DF.
fl uids and oral clarithromycin for 5 days.
Clinical features: We describe a young patient with
Outcome: Patient was discharged on day 8 of
DF who complained of sudden onset breathlessness
admission. She was well but follow-up BNP was
on day 3 of admission. She was found to have right
high but on downward trend. She refused any
sided crepitations. Myocardial screen was done
further invasive investigations for heart.
which was negative but BNP was 3555 pg/ml. Her
SpO and arterial blood gas while breathing room air
Conclusions: BNP may be raised in patient with
was normal. There was no elevated jugular venous
DF without heart failure. The exact pathogenesis of
pressure, pedal edema or laboratory evidence
raised BNP in DF is unclear.
Key words: Raised BNP, echocardiography, dengue fever, heart failure, renal impairment.
Introduction
Dengue fever (DF) is common in Singapore. We describe a young patient with DF with In Singapore, the total number of cases reported in brain natriuretic peptide (BNP) of 3555 pg/ml who was 2003 was 4788, giving an incidence rate of 114 per breathless with normal peripheral oxygen saturation 100,000 populations [1,2]. The numbers of cases of (SpO ) and arterial blood gas while breathing room air. DF reported in 2004 were 8500 with 1 death [3]. The There was no clinical or echocardiographic evidence number of cases in 2005 till September increased to of heart failure. Raised BNP in DF has not been Case Report
From Tan Tock Seng Hospital, Singapore (Drs. Ashish A. Sule, Dessmon YH Tai, Koh N. Yue, Veerendra Chadachan, Kenneth Ng).
Miss MML, a 30 year old Chinese lady, was Corresponding author:
hospitalised on 26/3/06 with moderate to high grade intermittent fever associated with chills and rigors. One day after onset of her fever, she developed itchy rash associated with sore throat and dry cough. She also had diarrhea 2 to 3 episodes and vomiting 2 episodes 1 day prior to admission. There was no Crit Care & Shock 2007. Vol. 10, No. 3 epistaxis or bleeding from any site. She had no other 40-200 U/L), CK-MB-mass 1.2 μg/L (normal 0.6-6.3 symptoms. There was no travel history. She was μg/L), troponin I 0.01 μg/L (normal 0-0.5 μg/L) and treated by general practitioner with clarithromycin for BNP was elevated at 3389 pg/mL (normal 0-100 pg/ 5 days with no improvement. She had no past history mL). Transthoracic 2-dimensional echocardiography of heart problems, hypertension or any other medical showed no evidence of heart failure (left ventricular or surgical illness. Her sister was recently admitted for ejection fraction 60%) or pulmonary hypertension (pulmonary artery systolic pressure 29 mmHg), normal On examination, patient was febrile (temperature 38 valves and cardiac chambers, trivial mitral and tricuspid °C), blood pressure (BP) 110/64 mmHg, heart rate regurgitation. Intravenous dextrose saline 1 litre per 90/minute. There was no lymphadenopathy. There day was continued. She was given oral clarithromycin was extensive maculopapular rash all over the body. 500 mg twice a day which was continued for 5 days.
Systemic examination did not reveal other abnormal On review the next day (29/3/06), her breathlessness had resolved. Full blood count showed haemoglobin 12.2 g/dL, white blood cells 5.7x109/L (neutrophils haemoglobin 12.9 g/dL, white blood cells 3.8x109/L 63.9%, lymphocytes 25.8%, monocytes 6.4%, (neutrophils 86.4%, lymphocytes 6.8%, monocytes eosinophils 3.2%), platelets 244x109/L. Her repeat 6.8%, eosinophils 0.5%), platelets 176x109/L. Serum electrolytes were normal, creatinine 55 μmol/L, urea T h e r e w a s a l s o n o c l i n i c a l o r 0.7 mmol/L, AST 63 U/L, ALT 66 U/L, albumin 32 electrocardiographic evidence of myocarditis. Deep g/L. Dengue IgM was positive and blood culture was vein thrombosis and pulmonary embolism were negative after 5 days of incubation.
unlikely as there was no calf swelling, no sinus Patient was diagnosed as dengue fever (DF). tachycardia on ECG, no hypoxia and no raised She was given symptomatic treatment and rehydrated pulmonary pressures on echocardiography. Hence, venous ultrasound doppler scan of the legs was not done as there was no clinical suspicion of deep vein she complained of breathlessness. There was no chest thrombosis. There was no clinical or laboratory pain, orthopnea or paroxysmal nocturnal dyspnoea. On examination, her vital signs were: BP 130/80 She was discharged well on 2/4/06. She was mmHg, heart rate 86/minute, SpO on room air was asymptomatic when she was followed up on 11/4/06 98%. She was afebrile. Her jugular venous pressure and BNP was still raised 1171 pg/mL. She refused any was not elevated. There was no pedal edema or unilateral leg swelling or tenderness. Auscultation of chest revealed few basal crepitations on the right. Discussion
Examination of the heart and abdomen was normal. Chest X-ray and electrocardiogram were normal. mosquito-borne viral infection of humans, affecting Arterial blood gas while breathing room air showed an estimated 100 million people worldwide each year. pH 7.48, PaCO 32 mmHg, PaO 136 mmHg, HCO It is endemic in parts of Asia and the Americas and 23 mmol/L, SaO 99%. Repeat full blood count on has been increasingly reported from many tropical 28/3/06 showed haemoglobin 11.7 g/dL, white blood countries in recent years. Dengue hemorrhagic fever cells 2.1x109/L (neutrophils 74%, lymphocytes 16.8%, (DHF) and dengue shock syndrome (DSS) are among monocytes 7.6%, eosinophils 0%, basophils 1.5%), the leading causes of hospitalization in Asia, with platelets 140x109/L, ESR 14 mm/hr, AST 310 U/L, up to 500,000 cases reported annually to the World ALT 230 U/L. In view of clinical chest fi ndings with Health Organization (WHO). Mortality rates from sudden onset shortness of breath, cardiac enzymes and <1% to 5% are usually quoted for DHF/DSS from BNP were done. The cardiac enzymes were negative centers experienced in fl uid resuscitation, but rates up for acute myocardial infarction: CK 175 U/L (normal to 44% have occasionally been reported in patients Crit Care & Shock 2007. Vol. 10, No. 3 with established shock. In Singapore, DHF was fi rst BNP is one of the members of a family of documented in 1960 when 70 hospitalised cases with structurally related peptides that participate in the 1 death were reported [1,2]. Since then, the disease integrated control of renal and cardiovascular function. has reached epidemic proportions at intervals of 1 to BNP is derived from 134-aa precursor prepro-BNP. 5 years. In Singapore there are 114 cases per 100,000 Upon release stimulation, a 26-aa signal peptide people and the total number of cases was 4788 in sequence is cleaved to produce pro-BNP. This is further 2003 [1,2]. The numbers of cases of DF reported in cleaved by membrane bound serine protease to produce 2004 were 8500 with 1 death [3]. The number of cases 32-aa peptide hormone termed BNP. This has a half life reported from January till September 2005 increased of 21 minutes and the release stimulus is ventricular to around 11,000 with 11 deaths [4].
wall tension. A persistently raised BNP in a patient with There are 4 serotypes of dengue virus, all of heart failure therefore indicates poor prognosis [6,7].
which may produce either a nonspecifi c febrile illness, BNP was initially identifi ed in the brain but is DF or may result in the more severe manifestation of also present in the heart, particularly the ventricles. The DHF. Guidelines for diagnosis of both DF and DHF plasma concentrations BNP are increased in patients are published by the WHO. DHF has been classifi ed with asymptomatic and symptomatic left ventricular into the following 4 grades of severity: grades I and dysfunction, permitting their use in diagnosis. A II involve only mild capillary leakage, insuffi cient plasma BNP >100 pg/mL diagnosed congestive heart to result in the development of shock, and are failure with a sensitivity, specifi city, and predictive differentiated by the absence (grade I) or presence accuracy of 90%, 76%, and 83% respectively. Plasma (grade II) of spontaneous bleeding; in grade III BNP concentrations are also elevated in patients circulatory failure occurs, manifested by a rapid, weak with pulmonary hypertension and right ventricular pulse, with narrowing of the pulse pressure to ≤20 dysfunction. In such patients, BNP levels correlated mmHg; in grade IV shock is severe, with no detectable positively with mean pulmonary artery pressure, total pulse or blood pressure. DHF grades III and IV are pulmonary resistance and right ventricular mass. A collectively referred to as DSS. For patients with DSS, high level of plasma BNP, and in particular, a further the WHO recommends immediate volume replacement increase in plasma BNP during follow-up may have with isotonic crystalloid solutions, followed by the use a strong, independent association with increased of plasma or colloid solutions (specifi cally, dextran) mortality in patients with primary pulmonary for profound or continuing shock. In the majority, hypertension [7]. Our patient had no clinical or however, the capillary leakage resolves spontaneously radiological evidence of pulmonary hypertension. BNP by the sixth day of illness and is followed rapidly is raised in systemic infl ammatory response syndrome by full recovery. In the 24-48 hour period following associated with cardiovascular dysfunction [8,9]. Our initial resuscitation, there may be recurrent episodes patient had no evidence of systemic infl ammatory of shock, presumably refl ecting the severity of the response syndrome. In patients with cor pulmonale (right heart failure), BNP can be high. It is also elevated in patients with renal impairment with left ventricular evidence of capillary leak syndrome. She received hypertrophy and fl uid overload [10,11]. Mark et al has intravenous dextrose saline (1 litre per day) from the described raised BNP in patients with renal failure day 1 of admission until she was discharged. She did in the absence of heart failure [12]. In our patient not develop any hypotension during hospital stay. She there was no renal impairment and/or fl uid overload had no clinical or echocardiographic evidence of heart secondary to renal impairment. Hyponatremia has been failure. Serum BNP was done in this patient when she shown in cerebral vasospasm following subarachnoid complained of breathlessness to exclude heart failure. haemorrhage (SAH). There is increasing evidence that Her SpO , arterial blood gas as well as 2-dimensional BNP is responsible for natriuresis after SAH. Sviri et echocardiography was normal. There was no evidence al showed that BNP was elevated shortly after SAH of pulmonary embolism or right heart strain.
for 1 week [13]. Inverse relationship has been shown Crit Care & Shock 2007. Vol. 10, No. 3 between BNP and body mass index (BMI) with heart 2. Brain tumor. Patient was asymptomatic and BNP failure. BNP is also found to be higher in females than was on downward trend. She refused further scans in males in cardiac failure and critically ill patients 3. Infi ltrative disorders of heart could not be excluded but patient was asymptomatic, she refused any The possibilities of raised BNP in this patient are: invasive investigations from cardiac point of view and BNP was on a downward trend.
1. Dengue fever. Raised BNP and its association with DF have never been described in literature. Further Conclusions
studies are needed to show whether DF without BNP may be raised in patients with DF in the heart failure is another cause of raised BNP, its absence of heart failure, renal failure or pulmonary pathogenesis and whether it has any prognostic hypertension. The exact pathogenesis of raised BNP and its prognostic value in DF are unclear.
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