Asian Pacific Journal of Tropical Medicine

CASE REPORT
Year
: 2022  |  Volume : 15  |  Issue : 4  |  Page : 179--182

Diffuse alveolar hemorrhage complicating dengue haemorrhagic fever in a 15-year-old boy: A case report


Prashant Gopal, Chaudhary Niraliben Hareshkumar, N.S.S. Saranya, Pradnya Diggikar 
 Department of General Medicine, Dr. D Y Patil Medical College, Hospital and Research Centre, Pune, India

Correspondence Address:
Pradnya Diggikar
Department of General Medicine, Dr. D Y Patil Medical College, Hospital and Research Centre, Pune
India

Abstract

Rationale: Dengue fever is a viral infection that is spread through the bites of infected female Aedes mosquitos. It can cause life threatening complications, including dengue haemorrhagic fever (DHF) and dengue shock syndrome. Patient concerns: A 15-year-old male presented with fever and petechiae and later developed hemoptysis. Diagnosis: Dengue fever with DHF with diffuse alveolar hemorrhage. Interventions: Invasive ventilation with high positive end expiratory pressure, multiple transfusions of packed red blood cells, fresh frozen plasma, single donor platelets and inotropic support Outcomes: The patient was stabilized and discharged on minimal supplemental oxygen. Lessons: Diffuse alveolar hemorrhage, although very rare, should be considered in a patient with dengue who presents with hemoptysis. The treatment is directed at providing respiratory and circulatory support, and preventing the progression of microcirculation damage.



How to cite this article:
Gopal P, Hareshkumar CN, Saranya N, Diggikar P. Diffuse alveolar hemorrhage complicating dengue haemorrhagic fever in a 15-year-old boy: A case report.Asian Pac J Trop Med 2022;15:179-182


How to cite this URL:
Gopal P, Hareshkumar CN, Saranya N, Diggikar P. Diffuse alveolar hemorrhage complicating dengue haemorrhagic fever in a 15-year-old boy: A case report. Asian Pac J Trop Med [serial online] 2022 [cited 2022 May 28 ];15:179-182
Available from: https://www.apjtm.org/text.asp?2022/15/4/179/340570


Full Text

 1. Introduction



Dengue fever is an arthropod-borne viral disease spread to humans through the bites of infected female Aedes mosquitos. Dengue virus is a positive-sense single stranded RNA virus that belongs to the Flavivirus genus (family Flaviviridae). Any of the four antigenically distinct serotypes (DEN-V 1-4) can cause infection[1]. It presents with non-specific symptoms such as fever, headache, and myalgia, making clinical diagnosis more difficult. To diagnose dengue infection, a combination of clinical and laboratory parameters (positive tourniquet test, relative bradycardia, leukopenia, and specific aspartate aminotransferase elevation with prolonged activated partial thromboplastin time) could be used as bedside markers[2]. Dengue virus can cause serious disease in humans, including dengue haemorrhagic fever (DHF) and dengue shock syndrome[3]. Minor to major bleeding, thrombocytopenia, and plasma leakage are signs of DHF. Epistaxis, gum bleeding, gastrointestinal bleeding, hypermenorrhoea, and haematuria are common hemorrhagic manifestations[4].

Lung involvement in dengue remains a contentious issue. In experimental infections and autopsies, viral antigens were detected in lung tissue, and the virus appears to be capable of infecting macrophages as well as lung endothelial and epithelial cells. Pleural effusion, pneumonitis, non-cardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), and hemorrhage/hemoptysis are possible pulmonary complications[1].

Diffuse alveolar hemorrhage (DAH) is a syndrome with several manifestations that can complicate various clinical conditions and can be life-threatening, necessitating urgent treatment. DAH symptoms include acute or subacute cough, hemoptysis, diffuse radiographic lung infiltrates, anaemia, and hypoxemic respiratory distress. This clinicopathologic condition is distinguished by the accumulation of intra-alveolar red blood cells arising primarily from alveolar capillaries but also from precapillary arterioles and postcapillary venules. DAH must be distinguished from localised pulmonary bleeding, which is typically caused by chronic bronchitis, bronchiectasis, malignancy, or localised infection[5].

 2. Consent for publication



Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

 3. Case report



A 15-year-old male presented with a five-day history of fever, headache, retro-orbital pain and myalgia. He had no cough, breathlessness, abdominal pain, nausea or vomiting. On examination, the patient was dehydrated, tachycardic with petechiae on bilateral arms and legs. Lab investigations revealed hemoglobin of 15.1 g/dL (haematocrit 45.4), platelets 35 000/dL, total leucocyte count was 3 300/dL, renal function tests were normal, aspartate aminotransferase was 149 units/L, albumin 2.7 g/dL, prothrombin time was 15.4 s and international normalized ratio (INR) was 1.3, C-reactive protein was 56 mg/L and ferritin was 1 896 ng/mL. Dengue NS1 was positive.

On the 2nd day, the patient developed multiple episodes of hemoptysis. He developed breathlessness and tachypnea (RR 34/min); oxygen saturation (SpO2) was 90% at room air. Chest auscultation revealed bilateral fine crepitations. Haematocrit dropped to 32.1 and platelets were 16 000/dL. High-resolution computed tomography thorax revealed bilateral peribronchovascular consolidations and ground glass opacities, predominantly in the left lung with mild bilateral pleural effusions (right>left) [Figure 1]. The patient underwent bronchofibroscopy, which showed the presence of blood-tinged secretions coming from bilateral lungs. Arterial blood gas was suggestive of type-1 respiratory failure with severe ARDS. The above clinical, laboratory and radiological findings were suggestive of DAH.{Figure 1}

On the third day of admission, patient was shifted to the intensive care unit and was transfused with two units of packed red blood cells, one unit of single donor platelets and four units of fresh frozen plasma. Intravenous tranexamic acid and vitamin K were added. Inotropes were started as blood pressure fell to 70/40 mmHg. He was intubated in view of respiratory distress and falling oxygen saturation levels. Intravenous antibiotics were started to prevent secondary infections. Haematocrit and platelet levels continued to drop over the next few days necessitating further transfusion of multiple units of packed red blood cells and single donor platelets along with intravenous calcium gluconate. Serum electrolyte levels were monitored daily and corrected as required. Patient required high positive end-expiratory pressure (PEEP) to maintain oxygenation levels. On the 7th day of admission, haematocrit levels stabilized and oxygenation levels improved [Table 1]. Hemoglobin and platelet levels were maintained above 10 g/dL and 50 000/dL respectively and the patient was weaned off ventilatory support on the 11th day. The patient continued to require oxygen supplementation and he was discharged once it was arranged at home. Incentive spirometry and regular follow-up for pulmonary function tests were advised. Three months after discharge, the patient did not require oxygen supplementation and is able to carry out daily routine activities.{Table 1}

 4. Discussion



The clinical presentation of dengue is varied ranging from non-specific febrile illness to dengue haemorrhagic fever and dengue shock syndrome[10]. A provisional diagnosis of DHF can be made based on the presence of a high fever with an acute onset, a positive tourniquet test, and hemoconcentration (a haematocrit increase of 20% or more) or thrombocytopenia[3].

Our patient fulfilled the WHO criteria for DHF since he presented with fever, haemorrhagic tendencies (petechiae and hemoptysis), thrombocytopenia and pleural effusion. Pleural effusion and pneumonitis are uncommon pulmonary manifestations in DHF, and pulmonary haemorrhage is even rarer. Hemoptysis has been reported in 1.4% of dengue infections. In DHF patients, the pathogenesis of bleeding is not well understood. The abnormalities in the coagulation cascade, thrombocytopenia, platelet dysfunction, disseminated intravascular coagulation, and vascular defects are thought to be part of a multifactorial process. Vascular permeability has been thought to be mediated by histamine release[3]. High- resolution computed tomography findings of our patient were suggestive of DAH, which may impede oxygen transfer, and resulting in hypoxemia. In this setting, the diffusion capacity of the lung for carbon monoxide may be increased, and serial increases in the diffusion capacity of the lung for carbon monoxide may indicate progressive alveolar hemorrhage. Interstitial fibrosis and restrictive changes may develop after recurrent episodes of DAH. Less commonly, patients may exhibit spirometric changes indicating airflow obstruction[5].

The treatment is directed at establishing the diagnosis, providing respiratory support, and preventing progression of microcirculation damage, typically with corticosteroids and immunosuppressive agents[6]. However, such treatment is potentially harmful when DAH is due to nonimmune causes such as infections[7]. In DHF, the treatment remains mainly supportive.

Acute hypoxemic respiratory failure is the most immediate life- threatening complication of DAH. When severe DAH results in ARDS, it is crucial to maintain an acceptable level of oxygenation using high levels of FiO2 and PEEP. Although no consensus exists regarding the optimal PEEP levels for DAH, they should be adjusted according to the severity of respiratory failure and lung recruitability. To control active bleeding and prevent lung collapse in patients with DAH, a high PEEP and permissive hypercapnia have been used[8].

To achieve rapid haemostasis, coagulopathy should be closely monitored and corrected as soon as possible. Platelet counts greater than 50 000/L and a prothrombin time-international normalised ratio less than 1.5 are commonly accepted targets. Platelet transfusions, vitamin K supplementation, cryoprecipitates, and fresh frozen plasma should all be supplemented, depending on the cause. To arrest the bleeding, various prothrombotic treatments have been used with varying degrees of success, including anti-fibrinolytics, particularly the lysine analogues tranexamic acid and epsilon aminocaproic acid, thrombin, and factor VIIa[9].

 5. Conclusions



DAH is a very rare presentation of DHF and the mainstay of treatment remains meticulous management of fluid and electrolyte balance with supportive care. The successful management of these patients requires a high index of suspicion, prompt evaluation, and appropriate therapy. DAH, although very rare, should always be considered in a patient with dengue who presents with hemoptysis.

Conflict of interest statement

The authors declare that there is no conflict of interest.

Funding

The authors received no extramural funding for the study.

Authors’ contributions

PD and PG performed the clinical diagnosis and treatments of the patient. NSS and CNH supervised the laboratory analysis and interpretation. NSS obtained the informed consent. PG, NSS and CNH monitored the patient, collected data and drafted the manuscript. PD revised and prepared the final version of the manuscript. All authors have read and approved the final manuscript.

References

1de Almeida RR, Paim B, de Oliveira SA, Souza AS, Gomes ACP, Escuissato DL, et al. Dengue hemorrhagic fever: A state-of-the-art review focused in pulmonary involvement. Lung 2017; 195(4): 389.
2Rao SM. Correlation of clinical and laboratory parameters in dengue fever patients and its usefulness as bedside markers. Indian J Crit Care Med 2014; 18(3): 183-184.
3Marchiori E, Ferreira JLN, Bittencourt CN, Neto CADA, Zanetti G, Mano CM, et al. Pulmonary hemorrhage syndrome associated with dengue fever, high-resolution computed tomography findings: A case report. Orphanet J Rare Dis 2009; 4(1): 8.
4Rao SV, Jacob GG, Raju NA, Ancheri S. Spontaneous arterial hemorrhage as a complication of dengue. Indian J Crit Care Med 2016; 20(5): 302-304.
5Von Ranke FM, Zanetti G, Hochhegger B, Marchiori E. Infectious diseases causing diffuse alveolar hemorrhage in immunocompetent patients: A state-of-the-art review. Lung 2013; 191(1): 9.
6Ioachimescu OC, Stoller JK. Diffuse alveolar hemorrhage: Diagnosing it and finding the cause. Cleveland Clin J Med 2008; 75(4): 258-280.
7De Prost N, Parrot A, Cuquemelle E, Picard C, Antoine M, Fleury-Feith J, et al. Diffuse alveolar hemorrhage in immunocompetent patients: Etiologies and prognosis revisited. Respir Med 2012; 106(7): 1021-1032.
8Kirby RR, Downs JB, Civetta JM, Modell JH, Dannemiller FJ, Klein EF, et al. High level positive end expiratory pressure (PEEP) in acute respiratory insufficiency. Chest 1975; 67(2): 156-163.
9Baineni R, Mallavarapu R, Devarapalli B prasad, Paturi VR. 1 586 diffuse alveolar hemorrhage in children with dengue fever: An observational study. Archiv Dis Childhood 2021; 106(Suppl 1): A422-A423.
10Singh S, Gupta A, Nanda SK, Devidas PD, Dwivedi D. Dengue fever leading to acute dengue hemorrhagic leukoencephalitis: A case report. J Acute Dis 2021; 10(6): 258-260.