Pathophysiology of acute falciparum malaria

Brooks, Marion H.; Malloy, John P.; Bartelloni, Peter J.; Tigertt, W. D.; Sheehy, Thomas W.; Barry, Kevin G.

doi:10.1016/0002-9343(67)90115-5

Cited by 45 publications

(9 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…BIA-determined TBW was significantly lower in those with severe compared with moderate malaria (mean [SD] of 539 [32] versus 562 [30] ml/kg, p = 0.034). TBW increased from admission to discharge in children with severe malaria by 37 (33) ml/kg or 6.7% (6.0%) (paired t test, p = 0.012), but there were no significant changes in TBW for children with moderate malaria between admission and discharge.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Assessment of Volume Depletion in Children with Malaria

et al. 2004

View full text Add to dashboard Cite

BackgroundThe degree of volume depletion in severe malaria is currently unknown, although knowledge of fluid compartment volumes can guide therapy. To assist management of severely ill children, and to test the hypothesis that volume changes in fluid compartments reflect disease severity, we measured body compartment volumes in Gabonese children with malaria.Methods and FindingsTotal body water volume (TBW) and extracellular water volume (ECW) were estimated in children with severe or moderate malaria and in convalescence by tracer dilution with heavy water and bromide, respectively. Intracellular water volume (ICW) was derived from these parameters. Bioelectrical impedance analysis estimates of TBW and ECW were calibrated against dilution methods, and bioelectrical impedance analysis measurements were taken daily until discharge. Sixteen children had severe and 19 moderate malaria. Severe childhood malaria was associated with depletion of TBW (mean [SD] of 37 [33] ml/kg, or 6.7% [6.0%]) relative to measurement at discharge. This is defined as mild dehydration in other conditions. ECW measurements were normal on admission in children with severe malaria and did not rise in the first few days of admission. Volumes in different compartments (TBW, ECW, and ICW) were not related to hyperlactataemia or other clinical and laboratory markers of disease severity. Moderate malaria was not associated with a depletion of TBW.ConclusionsSignificant hypovolaemia does not exacerbate complications of severe or moderate malaria. As rapid rehydration of children with malaria may have risks, we suggest that fluid replacement regimens should aim to correct fluid losses over 12–24 h.

show abstract

Section: Resultsmentioning

confidence: 99%

“…Hyponatraemia [30] has been attributed to high and possibly inappropriate arginine vasopressin secretion [31] in severe malaria. Our findings (high osmol gap, low ICW, and normal ECW) are more in keeping with sick cell syndrome than with inappropriate arginine vasopressin secretion [32,33].…”

Section: Discussionmentioning

confidence: 99%

Assessment of Volume Depletion in Children with Malaria

et al. 2004

View full text Add to dashboard Cite

show abstract

“…The malaria parasite is likely to determine the presence and degree of anaemia both directly by the abovementioned central and peripheral parasite effects, and also indirectly for example by inducing, through generalised vasodilation and internal fluid redistribution, complex changes in fluid balance resulting in the reduction of the effective circulating blood volume [32], which are corrected during recovery. It is therefore possible that, since what we measure is concentrations and not absolute numbers, we have an incomplete picture of the real situation in terms of both anaemia on presentation and recovery post-treatment.…”

Section: Discussionmentioning

confidence: 99%

Haemoglobin changes and risk of anaemia following treatment for uncomplicated falciparum malaria in sub-Saharan Africa

et al. 2017

View full text Add to dashboard Cite

BackgroundAnaemia is common in malaria. It is important to quantitate the risk of anaemia and to distinguish factors related to the natural history of disease from potential drug toxicity.MethodsIndividual-patient data analysis based on nine randomized controlled trials of treatments of uncomplicated falciparum malaria from 13 sub-Saharan African countries. Risk factors for reduced haemoglobin (Hb) concentrations and anaemia on presentation and after treatment were analysed using mixed effect models.ResultsEight thousand eight hundred ninety-seven patients (77.0% <5 years-old) followed-up through 28 days treated with artemisinin combination therapy (ACT, 90%, n = 7968) or non-ACT. At baseline, under 5’s had the highest risk of anaemia (77.6% vs. 32.8%) and higher parasitaemia (43,938 μl) than older subjects (2784 μl). Baseline anaemia increased the risk of parasitological recurrence.Hb began to fall after treatment start. In under 5’s the estimated nadir was ~35 h (range 29–48), with a drop of −12.8% from baseline (from 9.8 g/dl to 8.7 g/dl, p = 0.001); in under 15’s, the mean Hb decline between day 0–3 was −4.7% (from 9.4 to 9.0 g/dl, p = 0.001). The degree of Hb loss was greater in patients with high pre-treatment Hb and parasitaemia and with slower parasite reduction rates, and was unrelated to age. Subsequently, Hb increased linearly (+0.6%/day) until day 28, to reach +13.8% compared to baseline.Severe anaemia (<5 g/dl, 2 per 1000 patients) was transient and all patients recovered after day 14, except one case of very severe anaemia associated with parasite recurrence at day 28.There was no systematic difference in Hb concentrations between treatments and no case of delayed anaemia.ConclusionOn presentation with acute malaria young children with high parasitaemia have the highest risk of anaemia. The majority of patients experience a drop in Hb while on treatment as early as day 1–2, followed by a linear increase through follow-up. The degree of the early Hb dip is determined by pre-treatment parasitaemia and parasite clearance rates. Hb trends and rick of anaemia are independent of treatment. Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-017-2530-6) contains supplementary material, which is available to authorized users.

show abstract

“…Capillary injury was suggested by the frequent findings of dilatation and hyperemia of the septal capillaries by parasitized red cells [1,3]. Another hypothesis is that of generalized vasodilation which may result in decreased effective circulatory blood volume leading to an increase in aldosterone and antidiuretic hormone secretion to conserve sodium and water [7]. In addition, hypothalamic ischemia secondary to microthrombi within the hypothalamus with subsequent release of antidiuretic hormone has been postulated [1,3].…”

Section: Discussionmentioning

confidence: 99%

Acute Respiratory Failure Secondary to Falciparum Malaria

Dahmash

1993

Ann Saudi Med

View full text Add to dashboard Cite

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...

show abstract

Pathophysiology of acute falciparum malaria

Cited by 45 publications

References 10 publications

Assessment of Volume Depletion in Children with Malaria

Assessment of Volume Depletion in Children with Malaria

Haemoglobin changes and risk of anaemia following treatment for uncomplicated falciparum malaria in sub-Saharan Africa

Acute Respiratory Failure Secondary to Falciparum Malaria

Contact Info

Product

Resources

About