Severe hyponatraemia in an amiloride/hydrochlorothiazide-treated patient

A 85-year-old woman treated with, among other drugs, a thiazide diuretic presented with a severe hyponatraemia. She met several of the criteria for SIADH and, besides drugs, no cause for SIADH was found. After stopping the thiazide diuretic and restricting fluid intake the patient recovered fully. It was later proved that the thiazide was the cause of the water intoxication by rechallenging the patient with a single dose of amiloride/hydrochlorothiazide 5/50 mg. This "thiazide provocation test" showed its usefulness in the differential diagnosis of suspected SIADH. Moreover, the test demonstrated the paradoxal effect of thiazide diuretics to cause water retention in susceptible patients.     

ORIGINAL ARTICLE: Severe hyponatraemia in elderly hospitalized patients: prevalence,aetiology and outcome

Background: Hyponatraemia is the commonest electrolyte disorder in the elderly. Data on severe hyponatraemia and the prevalence of cerebral salt wasting syndrome (CSWS) in elderly hospitalized patients are lacking. We studied the incidence, frequency of various aetiologies, outcome and the possible role of CSWS in severe hyponatraemia in elderly medical patients. Methods: A prospective, observational, non‐interventional study conducted over a 5‐month period in medical wards. Eighty‐six patients aged over 65 years with serum sodium levels ≤125 mEq/L were included. All patients were examined by one of the authors, who also evaluated potential contributing factors. Demographic, clinical and outcome data were extracted from the medical records. Results: The mean age of the patients was 82.1 + 8.7 years. The prevalence of hyponatraemia was 6.2% (8.1% women and 4.0% men (P < 0.001)). There was no increase in incidence of hyponatraemia with age. The leading cause of hyponatraemia was the syndrome of inappropriate antidiuretic hormone secretion (SIADH), whose aetiology could be determined in only 46% of cases. Aetiology was multifactorial in 51% of patients (1.7 aetiological factors per patient). All patients with thiazide‐induced hyponatraemia had other contributing factors. Hyperglycaemia and hypoalbuminaemia were predictors of neurological manifestations of hyponatraemia. Overall in‐hospital mortality was 19%. Only hypoalbuminaemia was found as an independent risk factor for death. In none of the patients was the hyponatraemia due to CSWS. Conclusion: Severe hyponatraemia in elderly hospitalized medical patients is more frequent in women and of multifactorial aetiology in 50% of cases. It is most commonly caused by SIADH; CSWS is an unlikely cause.     

Severe hepatic dysfunction associated with falciparum malaria

We describe severe hepatic dysfunction associated with an attack of falciparum malaria in six Sri Lankan patients. Clinicians working in areas endemic for malaria should be made aware of this unusual complication.     

Tolterodine-induced hyponatraemia

Management of electrolyte abnormalities is challenging in older people as the sensation of thirst, renal function and hormonal modulators of the milieu interior are often impaired. Furthermore, the complex effects of ageing upon these homeostatic mechanisms are often superimposed upon a background of chronic disease, malnutrition and co-existent medications. Hyponatraemia is one of the commonest electrolyte abnormalities, occurring in approximately 7% of healthy elderly persons. Hyponatraemia may only come to light when some other ailment prompts investigations or hospital admission. Drug-induced hyponatraemia is common in older people and is most commonly associated with diuretics and SSRI/SNRI antidepressants, but has also been reported with a wide range of other drugs. We believe this is the first case report of hyponatraemia due to tolterodine.     

Severe anaemia in Zambian children with Plasmodium falciparum malaria

BACKGROUND: Severe anaemia and cerebral malaria are highly prevalent complications of Plasmodium falciparum malaria among African children. The mechanisms of severe malarial anaemia, and the relative importance of this condition in comparison to cerebral malaria, are not known for many regions of Africa. METHODS We reviewed the records of 6200 children up to 6 years of age admitted to one rural Zambian hospital between 1994 and 1996. Severe malarial anaemia was defined as an haemoglobin concentration < 5.0 g/dl in a patient with asexual forms of P. falciparum in the peripheral blood. Cerebral malaria was defined as impaired consciousness (Blantyre coma score < 5) not attributable to any other cause in a patient with a positive malaria smear. RESULTS Severe malarial anaemia was found in 590 children (9.5% of paediatric admissions) and strictly defined cerebral malaria occurred in 286 children (4.6% of paediatric admissions); 98 of these patients had the combination of both complications. Severe malarial anaemia correlated strongly with the degree of parasitaemia, with malnutrition as indicated by low weight for age, with absence of fever and with presentation late in the malaria season. In comparison, patients with cerebral malaria were more often febrile and presented earlier in the malaria season. The case fatality rate of severe malarial anaemia (0.088) was about half that of cerebral malaria (0.189), but because severe malarial anaemia was more common, these two forms of complicated malaria were implicated in similar numbers of in-hospital paediatric deaths. CONCLUSION Severe anaemia is a more common complication of P. falciparum malaria in hospitalized Zambian children than cerebral malaria and is associated with a similar number of deaths. Malnutrition and changes in immune response patterns due to prolonged exposure to P. falciparum may contribute to the development of this complication.     

Electrolyte derangement in cerebral malaria: a case for a more aggressive approach to the management of hyponatraemia

Although hyponatraemia has been consistently shown to occur in a large proportion of children with cerebral malaria, no statistical relationship has been established between the incidence of hyponatraemia and that of malaria-attributable mortality. However, hyponatraemia is not a benign state in other conditions (such as meningitis) or in surgical patients, and is likely to add to malarial deaths. The high mortality rate seen among cases of cerebral malaria, despite all efforts to curb it, therefore calls for a more aggressive approach to the management of hyponatraemia. Current methods for the administration of hypotonic saline and isotonic glucose solutions need review. In addition, children admitted with cerebral malaria should have their electrolyte status monitored to identify new or ongoing hyponatraemia. When hyponatraemia is discovered, it should be quickly and actively corrected.     

Severe falciparum malaria: survival without exchange transfusion

A case of severe falciparum malaria with trophozoites in 71% of the patients' erythrocytes is described. The patient was treated with high dose quinine and made an uneventful recovery. Exchange transfusion was not performed.     

Cyclophosphamide-induced symptomatic hyponatraemia

Cyclophosphamide is an alkylating agent used in antineoplastic and immunosuppressive therapies. Symptomatic hyponatraemia is a rare but life-threatening complication in patients treated with cyclophosphamide. We report the case of a 64-year-old woman with breast cancer who developed severe symptomatic hyponatraemia with a generalised seizure and convulsions after a second cycle of adjuvant chemotherapy with 5-fluouracil, epirubicin and cyclophosphamide. She completely recovered after correction of the serum sodium concentration without neurological deficits. Physicians prescribing cyclophosphamide, irrespective of the treatment indication and dosage, should be aware of this potentially life-threatening complication.     

Severe thrombocytopenia suggesting immunological mechanisms in two cases of vivax malaria

Case 1: A 27-year-old woman, referred to our hospital because of relapsing fever after travel to Thailand, was given a diagnosis of vivax malaria. Clinical investigation revealed thrombocytopenia, elevated platelet-associated IgG (PAIgG), and negative antibody against Plasmodium vivax antigen. After antimalarial treatment, the levels of both the platelets and PAIgG returned to normal. Case 2: A 28-year-old Sri Lankan man was admitted to our hospital with a complaint of fever. The patient had thrombocytopenia, elevated PAIgG, and positive antibody against Plasmodium vivax antigen. He contracted malaria in Sri Lanka about 6 months prior to this admission. After treatment, the platelet count and PAIgG level returned to normal. In these two cases, high levels of PAIgG may have been involved in the development of the thrombocytopenia. In the first patient, in particular, the thrombocytopenia was thought to be induced by some immunological mechanism prior to the detection of antimaralial antibodies in serum. Am. J. Hematol. 56:183–186, 1997. © 1997 Wiley-Liss, Inc.     

Severe anaemia in children living in a malaria endemic area of Kenya

Severe anaemia is an important cause of morbidity and mortality in African children, but the causes, particularly falciparum malaria, are difficult to determine. We assessed the contribution of falciparum malaria to anaemia in Kenyan children by clinical examination and measurement of parasitaemia and haemoglobin (Hb) concentration in 559 children in the community and in 2412 children admitted to Kilifi district hospital during a 2‐year period. We also attempted to characterize severe malarial anaemia by examining the causes and pathophysiology of anaemia in 101 children admitted with Hb concentration 50 g/l during a 1‐year period. Plasmodium falciparum infection was associated with reduced Hb concentration in children in the community and in those admitted to hospital irrespective of diagnosis. Falciparum malaria was the primary cause in 46 cases (46%) of severe anaemia admitted to hospital. There was no difference in the frequency of haemolysis or dyserythropoiesis in the children with malarial anaemia and those with anaemia from other causes, such as iron deficiency or sickle cell disease. The mortality rate in the children with severe malarial anaemia was 8.6% compared with 3.6% in children with severe anaemia due to other causes. Falciparum malaria does not present with a characteristic clinical or haematological picture, but is a major cause of the morbidity and mortality in children with severe anaemia who live on the Kenyan coast, a malaria endemic area.