|
 
 |
| CASE REPORT |
|
| Year : 2014 | Volume
: 16
| Issue : 1 | Page : 39-41 |
|
A case of severe falciparum malaria presenting with hyperglycemia
Yatendra Singh, Subhash C. Joshi, Vivekanand Satyawali, Abhisek Gupta
Department of Medicine, Government Medical College, Haldwani, Uttarakhand, India
| Date of Web Publication | 15-May-2014 |
Correspondence Address:
Dr. Yatendra Singh
Room No. 32, SR Hostel, Government Medical College, Haldwani - 263 139, Uttarakhand
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2276-7096.132579
Malaria remains a major cause of morbidity and mortality world-wide. World-wide more than 100 countries are endemic, but mainly in African and south East Asian region. We report a case of an uncommon presentation of Plasmodium falciparum infection in a 50-year-old male patient who presented with hyperglycemia and multiple organ dysfunction syndrome. Reports of unusual presentations of malaria are few and cases of severe malaria with hyperglycemia are rarely described. As hyperglycemia is associated to most severe malaria and high mortality, our aim is to draw the attention of the physicians on this entity. Keywords: Hyperglycemia, malaria, Plasmodium falciparum
How to cite this article:
Singh Y, Joshi SC, Satyawali V, Gupta A. A case of severe falciparum malaria presenting with hyperglycemia. J Med Trop 2014;16:39-41 |
| Introduction | |  |
An estimated 300-500 million people contract malaria each year, resulting in 1.5-2.7 million deaths annually. [1],[2] According to World Health Organization malaria report mortality decreased from 26.6 to 19.8 world malaria report 2011, incidence also decreased 65 per 1000 at risk. Elderly childrens and pregnant female who is at risk? In high-transmission areas, the risk for severe falciparum malaria is greatest among young children and visitors (of any age) from non-endemic areas. In other areas, severe malaria is more evenly distributed across all age groups. Risk is increased in the second and third trimesters of pregnancy, in patients with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome. In endemic regions, malaria can present with unusual features due to the development of immunity, increasing resistance to antimalarial drugs, and the indiscriminate use of antimalarial drugs. [3] As a result of lack of awareness of atypical manifestations, it is not uncommon for malaria to get diagnosed late or even go unrecognized, resulting in severe illness or death. We describe a case of severe Plasmodium falciparum malaria with hyperglycemia and multiple organ dysfunction syndrome (MODS). Although rare, this syndrome should be considered in patients brought to the emergency department in endemic areas. Exact mechanism of hyperglycemia is not known, but in malaria, the metabolic processes in the brain, including glucose uptake, are perturbed. Brain inflammation and increased expression of adhesion molecules of endothelial cells, red blood cells (RBCs), platelets and leukocytes result in the accumulation of these cells in the brain vessels. The resulting vascular occlusion and decreased blood flow damages the endothelium, leading to the blood brain barrier breakdown and leakage, with a resultant osmotic disequilibrium between the brain and plasma. [4] The resultant decreased glucose uptake and oxidation by the brain contributes to the hyperglycemia. In acute illness such as malaria several stress hormones and cytokines are released, which increase hepatic glucose production and insulin resistance. [5] All these contribute to hyperglycemia.
| Case Report | | |
The present case report is about a patient was a 50-year-old male of Northern India who had high grade fever associated with chills and rigors for 3 days. At 3 days after the onset of fever with recurrent vomiting episodes he referred to the family doctor and he was treated with antibiotic; malaria was not clinically suspected. There was no history of any other chronic illness or comorbid condition. On arrival in our hospital, the patient was dehydrated and pyrexial with a temperature of 102°F (38.9°C). Initial laboratory studies showed high creatinine level (256.36 μ mol/L or 2.9 mg/dL; reference range: 0.50-1.4 mg/dL), uremia (29.36 mmol/L or urea 176 mg/dL; reference range: 18-48 mg/dL), hyperglycemia (31.52 mmol/L or glucose: 568 mg/dL; reference range: 70-110 mg/dL), lactic acidosis (lactic acid: 3.6 mmol/L; reference range: 0.60-1.80), hypocalcemia (1.9 mmol/L or calcium: 7.8 mg/dL; reference range: 8.50-11.00 mg/dl), hyponatraemia (sodium: 126 mmol/L; reference range: 135-145), anemia (hemoglobin: 6.9 g/dL; reference range: 12.0-16.0) and thrombocytopenia (platelet count: 56,000/mm 3 ). His total leucocyte count was 9,000 cells/cumm with 70% neutrophils. The results of the rest of the routine blood tests including blood and urine culture were within normal limits. A blood smear detected a P. falciparum, with a density of 43% of parasitized RBCs. Malaria parasite (quantitative buffy coat) and malaria parasite card test (PfHRP2) test was positive for P. falciparum. A chest X-ray performed showed right lower lobe in homogenous opacity lobe pneumonia and moderate bilateral pleural effusion. The patient was screened for HIV, hepatitis B virus, hepatitis C virus, herpes simplex virus 1 and 2 and enteric fever, all investigations were negative. The patient was admitted to intensive care unit and he was treated for 5 days with intravenous (IV) artesunate (2.4 mg/kg stat iv followed by 2.4 mg/kg at 12 and 24 h and then daily), followed by artemether lumefantrine (1.5/9 mg/kg) twice a day for 3 day and for with IV ceftriaxone 1 g twice a day for 10 days. Antibiotic was given because suspicion of pneumonia and prevent from hospital acquired infection. Hyperglycemia was controlled by applying an intensive insulin protocol with a target glycemia of 150 mg/dL. He was transfused with 2 units of compatible packed red cells, 3 unit random platelet concentrates. At 24 h after starting artesunate the parasitemia decreased by 50% and less insulin was needed to achieve glucose control. Thick and thin smears obtained 72 h after therapy was negative for parasites. The insulin was injected subcutaneously according to blood glucose control after 5 days of presentation. He did not need insulin after 7 days. His fasting blood sugar was in the normal range along with other biochemical parameter when discharged after 10 days (blood sugar fasting 3 consecutive days less 3 mmol/L, urea-5 mmol/L, creatinine - 70 μ mol/L). He was in follow-up for 2 month and had persistently normal blood sugar levels.
| Discussion | | |
The classic presentation of malaria consists of paroxysms of fever. Symptoms usually associated with febrile paroxysms include shaking chills, sweats, headache, rigors, fatigue, malaise, arthralgia, myalgia, back pain, abdominal pain, nausea, vomiting, diarrhea, and jaundice. [6] However, classical presentation is seen in only 50-70% of the cases with the rest having atypical manifestations. [7] Some of the patients can develop features that suggest complications of malaria, usually caused by P. falciparum, such as cerebral malaria (CM) defined as coma or altered mental status, cerebellar ataxia or multiple seizures, seizures secondary to either hypoglycemia or CM, renal failure, severe anemia, thrombocytopenia, hypoglycemia, hemoglobinuria (blackwater fever), non-cardiogenic pulmonary edema, acute respiratory distress syndrome, renal failure, lactic acidosis, multiple organ dysfunction, bleeding (coagulopathy), and hemolysis resulting in severe anemia and jaundice.
It is important to be aware that malaria may present with unusual presentations. Uncommon presentations of malaria more frequent in P. falciparum malaria are acute abdomen, viral hepatitis-like illness, uremic encephalopathy, Guillain-Barr'e syndrome, severe headache, focal deficit (hemiplegia), urticaria, subacute intestinal obstruction, hyperglycemia, pancytopenia, pernicious syndrome, urinary frequency, relative bradycardia, and unexplained shock. [6],[7],[8] Respiratory manifestations of malaria include pleural effusion and lobar consolidation. Elevated pulmonary venous pressure secondary to venous and lymphatic obstruction by sequestration of infected RBCs, increased capillary permeability, and associated hypoalbuminemia are some of the mechanisms that have been proposed as the cause for pleural effusions. [9],[10]
Hyperosmolar hyperglycemic state most commonly occurs in patients with type 2 diabetes mellitus who have some concomitant illness that leads to reduced fluid intake. In general, any illness that predisposes to dehydration may lead to HHS. Infections are the major precipitating factor with urinary tract infections and pneumonia being the most common underlying causes of HHS. [11]
The exact prevalence of hospital hyperglycemia is not known, but it varies based on study populations and definition utilized in previous reports. Observational studies have reported prevalence of hyperglycemia ranging from 32% to 38% in community hospitals. [7],[9],[12],[13]
The American Diabetes Association and American Association of Clinical Endocrinologists consensus on inpatient hyperglycemia defined stress hyperglycemia or hospital-related hyperglycemia as any blood glucose concentration >7.8 mmol/L (140 mg/dL) without evidence of previous diabetes.
HSS is a potentially life-threatening emergency. Hospital treatment for HHS involves replacing the lost fluid caused by high glucose levels and the administration of insulin through a vein, to bring the blood glucose down to an acceptable level. It does not usually lead to the presence of ketones in the urine, as what occurs in ketoacidosis. Osier et al. reported that hyperglycaemia in the absence of insulin-dependent diabetes mellitus was present in 2.7% of children admitted to a rural Kenyan district hospital; the observational study included 3462 children outside the neonatal period and the commonest main primary diagnose was malaria (49.4%). [14] Moreover, they observed the mortality in hyperglycaemic children was higher than that in normoglycemic children. van Thien et al. in their study have reported the association of hyperglycemia with severe malaria and that CM stimulates glucose production to a greater extent than other forms of malaria. [15] Tombe et al. described one case of fatal severe malaria with hyperglycemia in a series of 33 patients. [16] Dass et al. saw two cases of hyperglycemia in malaria in a series of 162 cases who responded well to insulin therapy. [17] Eltahir et al. reported the hyperglycemia was frequent in severe malaria but more commonly associated with CM; the blood glucose levels were even higher in the fatal cases of CM. [18] According to the authors, the hyperglycemia was probably due to associated sepsis or a stress response with increased counter-regulatory hormones.
On arrival our patient was dehydrated and pyrexial. We believe that malaria and associated pneumonia have led to a range of responses: From increased counter regulatory hormones with hyperglycemia to a systemic inflammatory response which results in MODS. Prompt treatment with IV rehydration, IV artesunate, continuous IVs insulin, and ceftriaxone has led to clinical improvement. Hyperglycemia is a clinical entity not frequently reported in critically sick patients in contrast to hypoglycemia that is a more common finding and it is postulated to be caused both by the disease process and also secondary to quinine therapy. The physicians should focus their attention on this entity because the strong association between hyperglycemia and CM and/or other most severe form of malaria with high mortality detail a life-threatening form of severe diseases.
| References | | |
| 1. | Greenwood B, Mutabingwa T. Malaria in 2002. Nature 2002;415:670-2. 
|
| 2. | Krause PJ. Malaria (Plasmodium). In: Behrman RE, Kliegman RM, Jenson HB, editors. Nelson Textbook of Pediatrics. 18 th ed. Philadelphia, PA: WB Saunders; 2007. p. 1477-85.
|
| 3. | Singh UK, Kumar R, Sharma VK. Increased urinary frequency as a presentation of Plasmodium falciparum malaria. Pediatr Infect Dis J 1994;13:1024.
[PUBMED] |
| 4. | Zanini GM, Cabrales P, Barkho W, Frangos JA, Carvalho LJ. Exogenous nitric oxide decreases brain vascular inflammation, leakage and venular resistance during Plasmodium berghei ANKA infection in mice. J Neuroinflammation 2011;8:66.
|
| 5. | Dungan KM, Braithwaite SS, Preiser JC. Stress hyperglycaemia. Lancet 2009;373:1798-807.
|
| 6. | Taylor SM, Molyneux ME, Simel DL, Meshnick SR, Juliano JJ. Does this patient have malaria? JAMA 2010;304:2048-56.
|
| 7. | Zaki SA, Shanbag P. Atypical manifestations of malaria. Res Rep Trop Med 2011;2:9-22.
|
| 8. | Mohapatra MK, Padhiary KN, Mishra DP, Sethy G. Atypical manifestations of Plasmodium vivax malaria. Indian J Malariol 2002;39:18-25.
|
| 9. | Taylor WR, Cañon V, White NJ. Pulmonary manifestations of malaria: Recognition and management. Treat Respir Med 2006;5:419-28.
|
| 10. | Sirivichayakul C, Chanthavanich P, Chokejindachai W, Pengsaa K, Kabkaew K, Saelim R. Pleural effusion in childhood falciparum malaria. Southeast Asian J Trop Med Public Health 2000;31:187-9.
|
| 11. | Nugent BW. Hyperosmolar hyperglycemic state. In: Emergency Medicine Clinics of North America. Ch. 23. 2005. p. 629-48.
|
| 12. | Umpierrez GE, Isaacs SD, Bazargan N, You X, Thaler LM, Kitabchi AE. Hyperglycemia: An independent marker of in-hospital mortality in patients with undiagnosed diabetes. J Clin Endocrinol Metab 2002;87:978-82.
|
| 13. | Cook CB, Kongable GL, Potter DJ, Abad VJ, Leija DE, Anderson M. Inpatient glucose control: A glycemic survey of 126 U.S. hospitals. J Hosp Med 2009;4:E7-14.
|
| 14. | Osier FH, Berkley JA, Ross A, Sanderson F, Mohammed S, Newton CR. Abnormal blood glucose concentrations on admission to a rural Kenyan district hospital: Prevalence and outcome. Arch Dis Child 2003;88:621-5.
|
| 15. | van Thien H, Ackermans MT, Dekker E, Thanh Chien VO, Le T, Endert E, et al. Glucose production and gluconeogenesis in adults with cerebral malaria. QJM 2001;94:709-15.
|
| 16. | Tombe M, Bhatt KM, Obel AO. Clinical surprises and challenges of severe malaria at Kenyatta National Hospital, Kenya. East Afr Med J 1993;70:117-9.
|
| 17. | Dass R, Barman H, Duwarah SG, Deka NM, Jain P, Choudhury V. Unusual presentations of malaria in children: An experience from a tertiary care center in North East India. Indian J Pediatr 2010;77:655-60.
|
| 18. | Eltahir EM, El Ghazali G, A-Elgadir TM, A-Elbasit IE, Elbashir MI, Giha HA. Raised plasma insulin level and homeostasis model assessment (HOMA) score in cerebral malaria: Evidence for insulin resistance and marker of virulence. Acta Biochim Pol 2010;57:513-20.
|
|
Search Pubmed for