Acute Pulmonary Insufficiency in Falciparum Malaria: Summary of 12 Cases with Evidence of Disseminated Intravascular Coagulation

Punyagupta, Sompone; Srichaikul, Tanomsri; Nítiyanant, Prawat; Petchclai, B

doi:10.4269/ajtmh.1974.23.551

Cited by 102 publications

(45 citation statements)

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“…It was difficult to ascertain whether anaemia was due to malaria or some other disease like nutritional deficiency anaemia or worm infestation or gastrointestinal bleeding as previous reports of haemoglobin were not available in most of the patients. Many workers have reported high incidence of anaemia [25,26,27] in falciparum malaria. Normocytic and normochromic morphology of red blood cells was observed in 78% of cases which was similar to findings of White NJ et al [28] The pathophysiology of anaemia in malaria could be multifactorial envolving a complex series of interactions envolving destruction of parasitized red blood cells, ineffective erythropoiesis or immune mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Importance of Malarial Exclusion in a Thrombocytopenic Febrile Patient in an Endemic Area

Goel¹,

Vishwanathan²,

Mitra³

et al. 2015

jemds

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AIM OF THE STUDY:To evaluate the role of platelet count for predicting malarial infection and to determine the frequency and severity of thrombocytopenia in malarial parasite positive patients. STUDY DESIGN: The study included 150 patients who presented with fever in Santosh Medical College and Hospital, Ghaziabad. 97 patients with malaria were identified, rest were taken as control. Infection with both plasmodium vivax and plasmodium falciparum species was included. Thrombocytopenia was defined as platelet count less than 150000/cmm. RESULTS: Among 97 patients positive for malarial parasite, 78[80%] were found to have thrombocytopenia Overall 86 patients had plasmodium vivax while 8 patients had plasmodium falciparum infection and 3 had mixed infection. The frequency of thrombocytopenia was 78% [n=67] in vivax and 88% [n=7] in falciparum infection. Our study found the sensitivity of platelet count for diagnosing malaria was 80% and the specificity was 85%. Positive predictive value was 91% and negative predictive value was 83%. CONCLUSION: Platelet count can serve as an important initial screening tool in our setting. A finding of thrombocytopenia should increase the suspicion of malaria and more specific tests should be performed. Thrombocytopenia was a common haematological finding in patients with plasmodium infection, however its presence is not a distinguishing feature between the two types of malaria. Severe thrombocytopenia can occur in plasmodium vivax malaria although it is more common in plasmodium falciparum malaria.

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Section: Discussionmentioning

confidence: 99%

Importance of Malarial Exclusion in a Thrombocytopenic Febrile Patient in an Endemic Area

Goel¹,

Vishwanathan²,

Mitra³

et al. 2015

jemds

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“…The respiratory complications of malaria have recently been reviewed and range from benign forms such as bronchitis and pneumonia to fulminant respiratory failure secondary to rapidly progressive pulmonary edema [1][2][3][4][5][6]. It has been shown that the latter is due to noncardiac capillary permeability and may be rapidly fatal [1,3,5].…”

Section: Discussionmentioning

confidence: 99%

Acute Respiratory Failure Secondary to Falciparum Malaria

Dahmash

1993

Ann Saudi Med

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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...

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“…It is reported that the decreased platelet count in patients with malaria is related to shortening of the lives of platelets induced by excessive sequestration of platelets within the spleen (5-7). Someinvestigators (8) Pulmonaryedema has been reported by several investigators (3,9) to be one of the fatal complications of falciparum malaria. Fein et al (9) emphasized that pulmonary edema in patients with falciparum malaria is due to increased permeability of the alveolar-capillary membrane.…”

Section: Discussionmentioning

confidence: 99%

Falciparum Malaria in an Overseas Traveler Complicated by Disseminated Intravascular Coagulation and Pulmonary Edema.

et al. 1993

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A 24-year-old womanwas infected with falciparum malaria during travel to Kenya, complicated by intravascular coagulation and pulmonary edema. She was successfully treated with antimalarial drugs including chloroquine, quinine sulfate and pyrimethamine, with a combined regimen of heparin, antithrombin III and nafamostat mesilate for disseminated intravascular coagulation, and with methylprednisolone pulse therapy for pulmonary edema. The present case emphasizes the importance of early diagnosis and appropriate treatment in terms of falciparum malaria. This case, in particular, is believed to be worth reporting as overseas travel is increasing and yet anti-malarial drugs are not readily available to most physicians in Japan. (Internal Medicine 32: 395-398, 1993)

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Acute Pulmonary Insufficiency in Falciparum Malaria: Summary of 12 Cases with Evidence of Disseminated Intravascular Coagulation

Cited by 102 publications

References 0 publications

Importance of Malarial Exclusion in a Thrombocytopenic Febrile Patient in an Endemic Area

Importance of Malarial Exclusion in a Thrombocytopenic Febrile Patient in an Endemic Area

Acute Respiratory Failure Secondary to Falciparum Malaria

Falciparum Malaria in an Overseas Traveler Complicated by Disseminated Intravascular Coagulation and Pulmonary Edema.

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