Pulmonary Complications of Malaria

Patel, Vandana B.; Khan, Faroque A.

doi:10.1055/s-2007-1006220

Cited by 14 publications

(21 citation statements)

References 18 publications

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“…It has been shown that the latter is due to noncardiac capillary permeability and may be rapidly fatal [1,3,5]. We believe that our patient was in this particular category.…”

Section: Discussionmentioning

confidence: 54%

“…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%

“…Several mechanisms have been proposed to explain the increased alveolar capillary permeability in P. falciparum malaria [1,3]. The basic lesions appear to be severe disturbances in the pulmonary microcirculation secondary to microaggregation of parasitized red blood cells and subsequent injury to the capillaries of the lung [1,2].…”

Section: Discussionmentioning

confidence: 99%

“…Protean manifestations are well recognized [1][2][3]. Unusual presentation delays prompt diagnosis and effective management and leads to high fatality.…”

mentioning

confidence: 99%

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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 has been shown that the latter is due to noncardiac capillary permeability and may be rapidly fatal [1,3,5]. We believe that our patient was in this particular category.…”

Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Protean manifestations are well recognized [1][2][3]. Unusual presentation delays prompt diagnosis and effective management and leads to high fatality.…”

mentioning

confidence: 99%

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Acute Respiratory Failure Secondary to Falciparum Malaria

Dahmash

1993

Ann Saudi Med

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“…The patient had only a low parasitaemia, which disappeared on the second day of hospital admission. Furthermore, he did not present any of the criteria of severe malaria, such as cerebral malaria with coma or seizures, severe anaemia, oliguric renal failure, hypoglycaemia, malignant hyperthermia, acidaemia or acidosis, circulatory collapse or shock, spontaneous bleeding, disseminated intravascular coagulation, or jaundice [8,9]. Acute lung injury in malaria is also usually associated with a longer time interval to the initiation of adequate antimalarial therapy [10].…”

Section: Discussionmentioning

confidence: 99%

Pulmonary toxicity with mefloquine

Udry¹,

Bailly²,

Dusmet³

et al. 2001

European Respiratory Journal

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This report presents a case of acute lung injury developing within hours after administration of mefloquine for a low-level Plasmodium falciparum malaria, which was persistent despite halofantrine therapy. Extensive microbiological investigation remained negative and video-assisted thoracoscopic lung biopsy demonstrated diffuse alveolar damage. The evolution was favourable without treatment. This is the second report of acute lung injury and diffuse alveolar damage caused by mefloquine. Glucose-6-phosphate dehydrogenase deficiency was present in the former case and was thought to contribute to the lung injury. However, glucose-phosphate dehydrogenase was normal in the present case, suggesting that it is not a predisposing condition to the lung injury.

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Thrombotic microangiopathy associated with Plasmodium vivax malaria

et al. 2009

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Sirs, While severe malaria is usually associated with infection due to Plasmodium falciparum, there have been recent reports of life-threatening manifestations in patients with P. vivax infection. Acute renal failure (ARF) is reported to occur in 1-30% patients with falciparum malaria but rarely with vivax malaria [1][2][3]. We recently reported a case of P. vivax malaria with acute renal failure [3]. We now describe a boy with vivax malaria complicated by anemia, thrombocytopenia, ARF secondary to thrombotic microangiopathy, and acute respiratory distress syndrome.This 11-year-old boy presented with fever, with chills for 5 days, and abdominal pain, rapid breathing, hemoptysis and anuria for 3 days. There was no preceding history of diarrhea or dysentery. Investigations showed a hemoglobin level of 8.8 g/dl, leukocyte count of 7,800/mm 3 and platelet count of 10,000/mm 3 . A peripheral smear showed red cells parasitized with trophozoites of P. vivax (parasite count 200/μl); there was thrombocytopenia, but there were no fragmented red cells. His blood pressure was 120/70 mmHg, and oxygen saturation was 84%. The ratio of the partial pressure of oxygen in arterial blood to the inspired oxygen fraction (PaO 2 /FiO 2 ratio) was 150; a chest radiograph showed diffuse bilateral alveolar infiltrates, suggestive of acute respiratory distress syndrome. The blood level of urea was 239 mg/dl, creatinine 9 mg/dl, glucose 100 mg/dl, pH 7.12, bicarbonate 15 mEq/l, sodium 136 mEq/l and potassium 5 mEq/l. Urinalysis showed 3+ proteinuria and 80-100 red cells per high-power field; no casts or crystals were seen. Serum complement C3 was 46 mg/dl (normal 77-90 mg/dl); tests for antinuclear antibodies and antineutrophil cytoplasmic antibodies gave negative results. There was no evidence of disseminated intravascular coagulation. P. vivax malaria was confirmed by a specific polymerase chain reaction (PCR). Rapid detection test (Parascreen; Zephyr Biomedicals, Goa, India) and PCR gave negative findings for P. falciparum infection. Blood, urine and bronchoalveolar lavage cultures were sterile. Ultrasonography showed normal-sized kidneys with increased echotexture and ascites.The patient was treated with quinine, parenterally (10 mg/kg intravenously, 8 hourly), ceftriaxone and cloxacillin. He also received transfusions of packed red cells and platelets. Over the next 30 h, he underwent peritoneal dialysis for azotemia and metabolic acidosis. The parasite count dropped to nil, and the thrombocytopenia resolved 48 h after the initiation of intravenous (i.v.) treatment with quinine. While the respiratory distress rapidly improved, he continued to have oliguria and azotemia, requiring maintenance hemodialysis for 3 weeks. Five weeks after the onset of illness, the blood level of urea was 44 mg/dl, creatinine 1.1 mg/dl and C3 was 83 mg/dl.A kidney biopsy, during the second week of hospital stay, showed focal cortical necrosis with cortical edema. There was endothelial swelling and myo-intimal hyperplasia in the arterioles (Fig. 1). Immunoflu...

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Pulmonary Complications of Malaria

Cited by 14 publications

References 18 publications

Acute Respiratory Failure Secondary to Falciparum Malaria

Acute Respiratory Failure Secondary to Falciparum Malaria

Pulmonary toxicity with mefloquine

Thrombotic microangiopathy associated with Plasmodium vivax malaria

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