electronic-Perak Medical Journal. August 2019; Volume 1, Special Issue 2
Journal homepage: http://gids.mohe.gov.my/index.php/pmj
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CONFERENCE PROCEEDINGS
This abstract was submitted to Perak Research Conference 2019 20 August 2019
LEFT HYPOCHONDRIUM PAIN IN A DENGUE PATIENT WITH HEREDITARY SPHEROCYTOSIS: SEVERE DENGUE OR HEMOLYTIC CRISIS?
Lam Jo Ee, Christopher Sim Sze Bing
Medicine Department, Teluk Intan Hospital, Ministry of Health MALAYSIA
ABSTRACT
Keywords
dengue fever, hereditary spherocytosis, haemolysis NMRR-18-2333-44017
Correspondence to:
Lam Jo Ee
[email protected] Back to Content Page
INTRODUCTION AND OBJECTIVES
The presentation of anaemia and abdominal pain in a patient with dengue fever usually raise alarm bells for severe dengue. However, in patients with hereditary spherocytosis, infections including dengue fever could precipitate a haemolysis crisis which frequently manifest similar symptoms, as alluded in our report and differentiating them from symptoms of severe dengue is vital.
CASE PRESENTATION
A 16-year-old female, with hereditary spherocytosis diagnosed at 4 years old was admitted with four-day history of fever with chills, rigors, myalgia, tea coloured urine, diarrhoea and constant left lumbar pain. There was no shortness of breath or bleeding tendencies. Examination showed no evidence of shock or plasma leakage. Abdominal examination revealed tender splenomegaly. Initial haemoglobin was 7.7g/dL (HCT 19%; MCV 75.1 fL) and platelets of 82000/uL). Dengue NS-1 antigen test was positive. Full blood picture showed evidence of haemolysis, supported by serum bilirubin 165 µmol/L, lactate dehydrogenase 1537 U/L and reticulocyte count 11.0 %. Renal function, blood gases and serum lactate were normal. She was treated as dengue fever in febrile phase with no warning signs complicated with acute haemolysis. She was given maintenance drip. One pint of pack cells was transfused on day one of admission after the haemoglobin dropped to 6.7g/dL. On day two, her left hypochondriac pain worsened, requiring regular intravenous tramadol. Ultrasound abdomen revealed a distended gallbladder with pigment stones, minimal free fluid in pelvic cavity, and splenomegaly with no obvious thrombus within. Hepatic and portal veins were patent. She had no other warning signs and her vital signs remained stable. With further supportive management and analgesia, the haemolytic parameters continued to stabilise without further need for blood transfusion, and her intravenous drip was discontinued.
She subsequently made full recovery, with resolution of her left hypochondriac pain and haemolysis. She was discharged after six days with supplementary folate. On discharge, her haemoglobin 8.0g/dL, platelet count 122000/uL.
CONCLUSION
Haemolytic crisis is a known complication of hereditary spherocytosis and is usually triggered by environmental stressors, especially infection. In dengue fever, symptoms of haemolytic crisis may be misinterpreted as warning signs and it is vital to assess for both. In cases of severe splenic tenderness, imaging modalities such as ultrasound or computed tomography (CT) scan may be needed to rule out splenic thrombosis or collection. Supportive management usually leads to resolution of haemolysis and folic acid should be supplemented to prevent other complications such as megaloblastic crisis.
