Acute Respiratory Failure Secondary to Falciparum Malaria

Abstract

NS Dahmash, Acute Respiratory Failure Secondary to Falciparum Malaria. 1993; 13(5): 460-463 Malaria contributes enormously to the mortality and morbidity in many countries where it is endemic. Protean manifestations are well recognized [1][2][3]. Unusual presentation delays prompt diagnosis and effective management and leads to high fatality. While cerebral malaria, acute renal failure, and massive hemolysis are fairly common in frequency [2,3], malaria-induced respiratory failure is relatively rare [3]. We report a patient whose Plasmodium falciparum infection was complicated by rapidly progressive respiratory failure.A 25-year-old male from Sudan was well until 18 August 1989 when he presented to a hospital with a one week history of fever, chills, profuse sweating, and headache. A diagnosis of falciparum malaria was made and an oral chloroquine therapy was commenced. His clinical condition deteriorated with the development of nonproductive cough and vomiting and he was transferred to King Khalid University Hospital (KKUH). On admission to KKUH, physical examination revealed a very ill patient who was febrile (temperature 40°C), blood pressure 120/70 mm/Hg, pulse rate 110 per minute and a respiratory rate of 35 per minute. Examination of the cardiorespiratory system revealed bilateral crepitations, normal heart sounds without gallops or murmurs, and a normal jugular venous pressure. The spleen was palpable to 3 cm below the costal margin. Other systems were normal.Complete blood count revealed white blood count of 5.4x10 9 /L (polymorphonuclear cells 67%, bands 3%, lymphocytes 18%, monocytes 9%, eosinophils 1%, basophils 1%, atypical lymphocytes 1%), hemoglobin concentration of 13 g/dl, hematocrit 33%, and platelet count of 38,000. Prothrombin time 19 seconds (control 15 seconds) and the partial thromboplastin time was 35 seconds (control 23 to 33 seconds). Fibrinogen level was within the normal range and fibrinogen degradation products (FDP) were undetected. Blood glucose was 6 mmol/L, sodium 125 mmol/L, potassium 4.4 mmol/L, chloride 103 mmol/L, bicarbonate 23 mmol/L, blood urea nitrogen 4.9 mmol/L, and creatinine 84 μmol/L. His total bilirubin was 13 μmol/L (normal 0 to 17 μmol/L), direct bilirubin 1 μmol/L, total protein 56 g/L (normal 64 to 82 g/L), albumin 27 g/L (normal 34 to 50 g/L), serum aspartate aminotransferase (SGOT) was 148 u/1 (normal 0 to 35 u/L), serum aspartate alanine aminotransferase (SGPT) was 140 u/L (normal 0 to 35 u/L), alkaline phosphatase 95 u/L (normal 50 to 136 u/L and lactic acid level 2.5 mmol/L (normal 0.6 to 1.7 mmol/L). The result of urine analysis was unremarkable. Blood smear showed a significant load of P. falciparum. Sputum examination was unremarkable and subsequent culture grew no organisms. Special stain for acid fast bacilli and fungi was negative. Blood culture, brucella and typhoid titers were negative. Arterial blood gases obtained on room air were as follows: arterial oxygen tension (PaO 2 ) 41 mm/Hg, PCO 2 31 mm/Hg, pH 7.40, bicarbonate (HCO 3 ) 19 mmol/L, and...