Body fluid abnormalities in severe hyperglycemia in patients on chronic dialysis: review of published reports

Reports of dialysis-associated hyperglycemia (DH) were compared to reports of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH) in patients with preserved renal function. Average serum values in DH (491 observations), DKA (1036 observations), and NKH (403 observations) were as follows, respectively: glucose, 772, 649, and 961 mg/dl; sodium, 127, 134, and 149, mmol/l; and tonicity, 298, 304, and 355 mOsm/kg. Assuming that euglycemic (serum glucose, 90 mg/dl) values were the same (sodium, 140 mmol/l; tonicity, 285 mOsm/kg) for all three states, the hyperglycemic rise in the average serum tonicity value per 100-mg/dl rise in serum glucose concentration was 1.9 mOsm/kg in DH, 3.5 mOsm/kg in DKA, and 8.1 mOsm/kg in NKH. Neurological manifestations in DH patients were caused by coexisting conditions (ketoacidosis, sepsis, and neurological disease) in most instances, and by severe hypertonicity (>320 mOsm/kg), with clearing after insulin administration, in a few instances. In 148 episodes of DH corrected with insulin only, the mean increase in serum sodium per 100-mg/dl decrease in serum glucose (Delta[Na]/Delta[Glu]) was -1.61 mmol/l. In agreement with theoretical predictions, Delta[Na]/Delta[Glu] was numerically smaller in patients with edema than in those with euvolemia. The average hyperglycemic increase in extracellular volume, calculated from changes in serum sodium concentration during correction of DH using insulin alone, was 0.013 l/l per 100-mg/dl increase in serum glucose concentration. A small number of DH patients presented with pulmonary edema rectified by insulin alone. DH causes modest hypertonicity, with few patients having neurological manifestations caused usually by other coexisting conditions. In contrast to DKA or NKH, which usually presents with hypovolemia, DH causes hypervolemia manifested occasionally by pulmonary edema. Insulin is adequate treatment for DH.     

Nonketotic diabetes mellitus: Insulin deficiency or insulin resistance?

Ninety-five nonobese, nonketotic subjects were divided into five groups (one normal and four with varying degrees of glucose intolerance) according to their plasma glucose responses during an oral glucose tolerance test. These five groups were then compared on the basis of their insulin response during the oral glucose tolerance test and on the ability of exogenously infused insulin to limit hyperglycemia during a continuous infusion of glucose and insulin, while endogenous insulin was inhibited by the infusion of epinephrine and propranolol. The mean plasma insulin response of patients with either borderline abnormalities of glucose tolerance or chemical diabetes was equal to or greater than that of normal subjects at all points during the glucose tolerance test. Thus, the glucose intolerance of these two patient groups cannot be attributed to a lack of insulin. On the other hand, the mean insulin response of patients with moderate fasting hyperglycemia (plasma glucose of 110 to 150 mg/100 ml) was somewhat attenuated, and patients with severe fasting hyperglycemia (plasma glucose > 150 mg/100 ml) had unequivocal insulin deficiency. In contrast, all four patient groups with abnormal carbohydrate metabolism were more resistant than normal subjects to the action of insulin. These results indicate that there is a very complex relationship between insulin deficiency and insulin resistance in patients currently classified as having nonketotic diabetes. Patients with either borderline abnormal glucose tolerance or chemical diabetes are more resistant to insulin than normal subjects, and are not insulin deficient. In these patients it seems reasonable to assume that their glucose intolerance is a direct function of their insulin resistance. Patients with severe fasting hyperglycemia are suffering from both insulin deficiency and insulin resistance, and the relationship between these two variables in the genesis of hyperglycemia in these subjects remains obscure. It seems apparent from these studies that nonketotic diabetes mellitus can no longer be considered to be a simple function of insulin lack, and that in order to understand this syndrome we will need to increase our knowledge of the relationship between insulin deficiency and insulin resistance in these patients.     

Cerebral edema in children with diabetic ketoacidosis

Cerebral edema is the most frequent serious complication of diabetic ketoacidosis (DKA) in children, occurring in 1% to 5% of DKA episodes. The rates of mortality and permanent neurologic morbidity from this complication are high. The pathophysiologic mechanisms underlying DKA-related cerebral edema are unclear. A number of past and more recent studies have investigated biochemical and therapeutic risk factors for the development of cerebral edema. Recent studies have shown that a higher initial serum urea nitrogen concentration and lower initial partial pressure of carbon dioxide are associated with the development of cerebral edema. This and other information suggests that the pathophysiology of DKA-related cerebral edema may involve cerebral ischemia.     

Computer analysis of magnetic resonance imaging of the brain in children and adolescents after treatment of diabetic ketoacidosis

Cerebral vascular accidents are one of the causes of morbidity and mortality in children with diabetic ketoacidosis. We investigated the possible occurrence of asymptomatic cerebrovascular infarcts and the course of subclinical brain edema in six patients. Neurologic examinations and computer analysis of magnetic resonance imaging were performed immediately after, and again at 14 days after, correction of DKA. None of the patients had clinical evidence of a neurologic deficit. Neither radiologic evaluation nor computer analysis of MRI identified changes indicating asymptomatic ischemic events. However, a computer analysis of the MRI identified a significant increase of the total ventricle area between Day one and Day 14. Our study does not establish whether this change is a return to the baseline prior to DKA or a new baseline, representing an early manifestation of diabetic encephalopathy.     

Hyperosmolar nonketotic coma with hyperglycemia: abnormalities of lipid and carbohydrate metabolism

Severe hyperglycemia may occur without ketosis and may lead to dehydration, coma, and death in patients with mild diabetes mellitus. To elucidate the biochemical mechanisms, measurements of plasma insulin, free fatty acid, and growth hormone were made before treatment in 15 comatose hyperglycemic patients without ketosis. Fatty acids, markedly elevated and the source of ketones in ketoacidosis, were normal in nonketotic coma. Lack of mobilization of fat seems not to be related to growth hormone secretion since the plasma levels of this hormone ranged from very low to high and did not correlate with glucose or acetone. Plasma insulin, which is reported to be almost absent in ketoacidosis, was found at levels thought to be capable of suppressing lipolysis without preventing hyperglycemia. Dehydration and hyperglycemia probably play a secondary role in prevention of fat mobilization and ketone production.     

Posterior reversible encephalopathy syndrome (PRES) and chronic kidney disease

Posterior reversible encephalopathy (PRES) is a recently described syndrome, defined by clinical and neuroimaging features. Chronic kidney disease patients may be especially vulnerable to this syndrome because they are frequently exposed to several of its possible causes, including uremia and hypertension. In its most severe form, PRES can manifest clinically as seizures, coma or death. However, if properly diagnosed and treated, this syndrome can be completely reversible. Therefore, neuroimaging methods, especially brain magnetic resonance is fundamental for its diagnosis because it shows brain edema in characteristic pattern, and excludes causes of seizures or coma. An important example is the case of a young hypertensive chronic kidney disease patient on peritoneal dialysis, brought to the emergency room comatous with generalized tonic-clonic seizures; the cerebral magnetic resonance imaging features were impressive. Anti-hypertensive therapy and hemodialysis allowed complete recovery. The reversibility of this syndrome depends on timely diagnosis and therapy and therefore it should be kept in mind in the differential diagnosis of seizures. or coma in chronic kidney disease patients.     

Hyperosmolar nonketotic diabetic coma: a complication of propranolol therapy

A 46-yr-old hypertensive man treated for 1 yr with apresoline 200 mg and propranolol 240 mg daily, was admitted in deep coma, severely dehydrated, serum glucose $\text{1130}\text{mg}\text{100}\text{ml}$ without ketonemia, normal serum CO₂, blood pH 7.52, serum osmolarity 357 mOsm/kg, fever of 105.6°F, and central venous pressure of less than 1 cm. The plasma free fatty acid was 270 μeg/liter, insulin 16 μU/ml and growth hormone 2.5 ng/ml. He responded excellently to 100 units regular insulin and 8 liters of hypotonic infusions. Seven months later he had a similar episode despite addition of 1 g tolbutamide daily in the interim. When studied without any medication he had fasting hyperglycemia of $\text{175–200}\text{mg}\text{100}\text{ml}$. An intravenous tolbutamide test was diabetic. When repeated following intravenous propranolol, 10 mg, the insulin response to tolbutamide was diminished. Without propranolol or hypoglycemic therapy, fasting hyperglycemia increased over 5–6 wk to $\text{630}\text{mg}\text{100}\text{ml}$, with traces of ketonemia, FFA level of 1350 μeq/liter and serum osmolarity of 305 mOsm/kg. The study was later repeated with the addition of oral propranolol 240 mg daily. Uncontrolled diabetes was again clinically manifest, although glucose levels rose more slowly. Despite fasting glucose levels reaching $\text{930}\text{mg}\text{100}\text{ml}$, no sign of ketosis occurred when the patient was taking propranolol. FFA level at this time was only 640 μeq/liter and serum osmolarity had risen to 335 mOsm/kg. His diabetes is now satisfactorily treated with insulin injections, to avoid the disturbances of carbohydrate metabolism caused by propranolol. These studies indicate that large amounts of propranolol may precipitate hyperosmolar nonketotic coma in an untreated diabetic by a blockade of lipolysis and/or impairment of insulin response.     

高渗性非酮症糖尿病昏迷的血液透析治疗

目的:探讨血液透析救治高渗性非酮症糖尿病昏迷(HNDC)的疗效及临床应用适应证。方法:将36例HNDC患者随机分为2组,观察组19例,采用血液透析和一般疗法相结合治疗;对照组17例,采用一般治疗方法,包括输液、小剂量胰岛素应用、纠正电解质紊乱和抗感染等。观察两组患者治疗前和治疗后4、12、24、48、72h血生化指标、血浆渗透压的变化及患者清醒时间、并发症和病死率。结果:观察组治疗后4、12、24、48、72h血糖、血钠、血尿素氮、血浆渗透压均明显降低(P<0.05),患者清醒时间早,并有效地降低了心力衰竭、脑水肿、肺水肿的发生,降低了死亡率。观察组较对照组疗效明显(P<0.05)。结论:血液透析是临床救治HNDC的有效方法之一。     

Factors associated with mortality in children with diabetic ketoacidosis (DKA) in South India

Mortality in diabetic ketoacidosis (DKA) among children has been reported to be 0.3–3 % in developed countries. Based on the limited data from developing countries, the mortality reported is as high as 13.4 %. A prospective study was conducted to identify the factors leading to high mortality in children with DKA in South India. This was a study of 118 episodes of DKA among children, admitted in a pediatric tertiary care center at Chennai. Clinical presentation, laboratory parameters at admission, parameters during treatment, and complications were considered as risk factors. All children were followed up till discharge from hospital or death. Univariate and multivariate analyses for risk factors were undertaken. Altered sensorium and higher osmolality at admission, delayed diagnosis, cerebral edema, shock, renal failure, and sepsis were the major risk factors associated with mortality in multivariate analysis. Cerebral edema was encountered in 23.7 %, shock in 12.7 %, sepsis in 11 %, and renal failure in 9.3 %. The overall mortality rate was 11 %. Delayed diagnosis may be the root cause for high mortality in children with DKA in developing countries. There is an urgent need to create awareness among physicians, teachers, and parents to avoid a delay in diagnosis and decrease the mortality in children with DKA. Higher incidence of cerebral edema, shock, renal failure, and sepsis are unique problems identified in this study. There is a need for further studies on fluid management of shock, strategies for management of renal failure in DKA, and use of antibiotics in DKA in developing countries.     

Hormone and metabolic profile in diabetic hyperosomolar coma. Plasma insulin response to intravenous tolbutamide (author's transl)]

Fifteen patients with non-ketotic hyperosmolar diabetic coma were investigated and compared with ketoacidotic patients. Basal plasma insulin levels were low in all patients (14.8 +/- 1.0 micronU/ml in hyperosmolar coma, 11.0 +/- 1.3 in keto-acidosis), but insulin level increased after intravenous tolbutamide (between 30 and 105 micronU/ml) in eight hyperosmolar comas. Insulin showed no increase in seven hyperosmolar comas and in none of the ketoacidotic patients. In hyperosmolar coma plasma free fatty acids (1710 +/- 197 micronEq/1), triglycerides (3,4 +/- 0,4 g/1) and cortisol levels (49,7 +/- 9,0 microgram/100 ml) were increased, must as in keto-acidosis. Growth hormone (1,7 +/- 0,1 ng/ml) was normal, unlike the case in keto-acidosis. Plasma lactate concentrations were elevated and account for the frequent mild acidosis found in hyperosmolar coma. In spite of the low peripheral "insulin/glycemia ratio", the positive response to tolbutamide in half of the hyperosmolar cases suggests a less complete pancreatic deficiency than in keto-acidosis. The plasma high free fatty acid and triglyceride levels suggest that the lack of ketosis is not due to inhibition of lipolysis but could be a consequence of inhibition of hepatic ketogenesis.     

Determinants of glucose and ketoacid concentrations in acutely hyperglycemic diabetic patients

Diabetic hyperosmolar coma is a syndrome of marked hyperglycemia and minimal ketoacidosis. In general, the serum glucose concentrations are not predictive of the serum ketoacid concentrations in acutely decompensated diabetes. The endocrine factors that modulate glucose concentrations may be different from those that modulate ketoacid concentrations in patients with acutely decompensated diabetes. To test this hypothesis, regression analysis was used to determine the endocrine and metabolic characteristics that correlated with serum concentrations of glucose and ketoacids in 26 diabetic patients with spontaneous, acute hyperglycemia. All patients had a serum glucose level greater than 390 mg/dl, and ketoacid levels were from 0.17 to 25.5 mM. Multiple regression analysis showed that increased serum glucose concentrations correlated with increased plasma glucagon levels (p = 0.0007, r2 = 0.45), but with no other factors. Increased total ketoacid levels (acetoacetate plus 3-hydroxybutyrate) correlated with increased free fatty acid levels (p = 0.0001), decreased C-peptide levels (p = 0.002), and increased body mass index (p = 0.002) (r2 = 0.72). Body mass index only correlated with ketoacid levels, when it was analyzed with C-peptide and free fatty acid levels. A model is proposed that predicts the serum glucose and ketoacid concentrations in patients with acutely decompensated diabetes. Glucagon modulates the serum glucose concentration in these patients with an absolute or relative insulin deficiency. Total serum ketoacid levels are determined by the serum free fatty acid concentration, residual pancreatic insulin secretion (as reflected by C-peptide), and the patient's body habitus. This model allows for the marked hyperglycemia and minimal ketosis of diabetic nonketotic hyperosmolar coma, as well as the glucose and ketoacid concentrations in other presentations of acutely decompensated diabetes.     

Acetoacetate and beta-hydroxybutyrate differentially regulate endothelin-1 and vascular endothelial growth factor in mouse brain microvascular endothelial cells.

Insulin-dependent diabetes mellitus (IDDM), is characterized by a lack of insulin production from beta cells in the pancreas. One of the metabolic consequences of this insulin deficit is an increased hepatic synthesis of ketone bodies, resulting in a serious medical complication, diabetic ketoacidosis (DKA). DKA, in turn, has been associated with the development of cerebral edema. The severity of this complication ranges from death to a subclinical presentation, but seems to be invariably present to some degree. The etiology of the cerebral edema is unknown, but changes in osmolality, pH, and insulin effects on the blood-brain barrier have all been suggested as possible culprits. Blood-brain barrier impermeability is maintained by the endothelial cells (EC) lining the blood vessels. Thus, it would seem likely that alterations in EC function would be necessary for the development of cerebral edema. However, no studies have examined the effects of ketone bodies on brain endothelial cells. The two major ketone bodies in DKA are acetoacetate (AcAc) and beta-hydroxybutyrate (BOHB). In the present study we examined the effect of these ketone bodies on a major intracellular signalling pathway. The changes in intracellular calcium concentration, and the production of two vasoactive peptides, endothelin-1 (ET-1) and vascular permeability factor (VPF/VEGF) in mouse brain microvascular endothelial cells (MBMEC). The present studies demonstrate the BOHB can increase vascular permeability factor. In contrast, AcAc increases the production of the potent vasoconstrictor, endothelin-1. This data would suggest that brain ECs are potential targets of the metabolic alterations in DKA.     

Reversible long-term tachycardia and hypertension as a symptom of autonomic neuropathy in combination with sensorimotor polyneuropathy in a patient with newly discovered type 1 diabetic mellitus

The case of 22 years old woman admitted with ketoacidotic coma and newly diagnosed insulin dependent diabetes mellitus is described. The signs of mixed sensoromotoric polyneuropathia in this patient have been discovered. After the correction of ketoacidotic hyperglycemic coma the significant tachycardia and hypertension with the abnormalities of diurnal rhythm with necessity of the intensive treatment persisted for the period of the several monthes. These changes we attributed to the significant dysfunction of the autonomic system. In the course of 1 year of good diabetes compensation the above mentionned hemodynamic changes subsided completely. In the same time the signs of mixed polyneuropatia and the incipient retinopathia disappeared. The causes of the described changes are discussed, mainly the importance of reversible microvascular changes.     

A case of systemic lupus erythematosus with extensive brain stem involvement

Systemic lupus erythematosus (SLE) is a multisystem, autoimmune connective tissue disorder. Neuropsychiatric SLE (NPSLE) has varied clinical and radiological manifestations. Clinical manifestations range from subtle abnormalities of neurocognitive functions and mood changes to overt psychiatric or neurological manifestations such as seizures, stroke, and psychosis. Magnetic resonance imaging (MRI) may show various types of abnormalities. Cerebral white matter lesions are most common (60–86%). Here, we are discussing a young female who presented with alteration of sensorium and right-sided hemiparesis, and MRI of the brain showed extensive involvement of brainstem in the form of possible demyelination.     

Investigation of insulin resistance during diabetic ketoacidosis: role of counterregulatory substances and effect of insulin therapy.

It has been generally accepted that insulin resistance (IR) exists in diabetic subjects during episodes of ketoacidosis (DKA). However, little experimental data exist regarding this question. We have studied IR in nine untreated diabetic subjects (mean age 20 yr) both during their initial episode of DKA and after 2–7 wk of insulin therapy. The experimental protocol consisted of a 150-min intravenous infusion of glucose (6 mg/kg/min) and insulin (80 mU/min). Under these conditions steady-state plasma glucose (SSPG) and insulin (SSPI) levels were reached by 90 min and maintained for the duration of the study. Since all subjects achieved similar SSPI and all received the same glucose load, the SSPG could be used as a measure of an individual's IR. In addition, steady-state plasma levels of glucagon, cortisol, growth hormone, and free fatty acids were measured in an attempt to gain insight into their roles in the maintenance of IR during DKA. Although mean (± SE) SSPI levels were the same during both study periods (93 ± 4 versus 92 ± 4 μU/ml), there was a marked difference between the initial and posttherapy SSPG levels for the nine subjects 342 ± 32 versus 104 ± 16 mg/100 ml,p < .001). Mean steady-state plasma levels of growth hormone, corticol, and free fatty acids were significantly higher during the initial studies, but only cortisol and free fatty acid levels correlated significantly with their corresponding SSPG levels. Steady-state plasma glucagon levels were the same during both study periods, and individual levels did not correlate with associated SSPG levels. These studies demonstrate that significant IR was present in these subjects during DKA as compared to the posttherapy period. Furthermore, the results suggest that while increased plasma concentrations of cortisol and free fatty acids may be involved in the maintenance of IR during DKA, elevated levels of plasma growth hormone and glucagon are not necessary for this phenomenon.     

A case of systemic lupus erythematosus with extensive brain stem involvement

Systemic lupus erythematosus (SLE) is a multisystem, autoimmune connective tissue disorder. Neuropsychiatric SLE (NPSLE) has varied clinical and radiological manifestations. Clinical manifestations range from subtle abnormalities of neurocognitive functions and mood changes to overt psychiatric or neurological manifestations such as seizures, stroke, and psychosis. Magnetic resonance imaging (MRI) may show various types of abnormalities. Cerebral white matter lesions are most common (60–86%). Here, we are discussing a young female who presented with alteration of sensorium and right-sided hemiparesis, and MRI of the brain showed extensive involvement of brainstem in the form of possible demyelination.     

Diabetic coma: Serum growth hormone before and during treatment

Summary Serum growth hormone values in 37 patients with diabetic ketoacidosis were 5.4±0.8 ng/ml (S.E.M.) in males and 6.7±1.1 ng/ml in females before treatment; while in five hyperosmolar non-ketotic patients the HGH concentration was 3.9±0.5 ng/ml. One hour after insulin 90% of patients showed a rise in HGH, to a mean of 33.7±9.8 ng/ml for males and 25.5±6.0 ng/ml for females in ketoacidosis; and to 27.1±9.9 ng/ml for hyperosmolar coma patients. The rise, which was transient, was inversely correlated with pretreatment plasma glucose, the l h plasma glucose concentration and plasma urea, and directly proportional to the % fall in blood glucose after 1 h. When the ketoacidosis patients were divided into two groups according to HGH response, those with a small response had the greater disturbances of plasma glucose, blood ketone bodies, blood lactate, plasma urea, blood pH, and blood pressure, the smaller 1 h fall in blood glucose, and the higher mortality. Thus the most severely ketoacidotic patients had the poorest growth hormone response. Growth hormone is probably of little importance as an insulin antagonist in diabetic coma.Presented in part at the Spring Meeting of the British Diabetic Association, York, April 1972.     

Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes.

1. An attempt was made to evaluate the pathophysiology of symptoms of hyponatremia as related to changes in brain water and electrolytes. Studies were carried out in 66 hyponatremic patients and 5 groups of experimental animals. 2. In hyponatremic patients, symptoms (depression of sensorium, seizures) correlated well with plasma Na+ (r = 0.64, p less than .001), but there was substantial overlap. In patients with acute hyponatremia, all were symptomatic and 50% died. Among patients with hyponatremia of at least 3 days duration, sympatomatic patients had plasma Na+ (115 +/- 1 mEq/L) which was significantly less (p less than .001) than that of asymptomatic patients (plasma Na+ = 122 +/- 1 mEq/L). Among symptomatic patients, mortality was 12% and 8% had seizures, while none of the asymptomatic patients died or had seizures. 3. Among 14 patients with acute (less than 12 hrs) hyponatremia, the mean plasma Na+ was 112 +/- 2 mEq/L. All such patients had some depression of sensorium and four had grand male seizures. Seven of these patients were treated with hypertonic (862 mM) NaCl, while four were treated only with fluid restriction. Of the seven patients treated with hypertonic NaCl, five survived, while three of four patients treated with fluid restriction died. There was no evidence of circulatory congestion or cerebral damage in the patients treated with hypertonic NaCl. 4. Among rabbits with acute (2-3 hours) hyponatremia (plasma Na+ = 119 +/- 1 mEq/L), all had grand mal seizures and 86% died. All such animals had cerebral edema (brain H2O content 17% above control value) but brain content of Na+, K+ and Cl- was normal. 5. Rabbits with 3 1/2 days of hyponatremia (plasma Na+ = 122 +/- 2 mEq/L) appeared to be asymptomatic, even though brain water content was 7% above normal (p less than .01). 6. Rabbits with 16 days of more severe hyponatremia (plasma Na+ = 99 +/- 3 mEq/L) were weak, anorexic, lethargic and unable to walk. Brain water content was 7% above normal, although brain osmolality (218 +/- 12 mOsm/kg H2O) was similar to plasma (215 +/- 8 mOsm/kg). Brain content of Na+, K+, Cl- and osmoles was 17 to 37% less than normal values, so that the brain established osmotic equilibrium with plasma primarily by means of a loss of electrolytes. 7. These studies suggest that in patients with hyponatremia, symptoms and morbidity are only grossly correlated with either magnitude or duration of hyponatremia. Symptoms appear to correlate best with the interplay between a net increase in brain water versus a loss oof brain electrolytes. However, even asymptomatic animals have subclinical brain edema when plasma Na+ is below 125 mEq/L, and such edema may cause permanent brain damage. Thus, many patients with similar levels of plasma Na+, particularly when they are symptomatic, should probably be treated with hypertonic NaCl infusions.     

Cerebral oedema during treatment of diabetic ketoacidosis: are we any nearer finding a cause?

Cerebral oedema remains the leading cause of death and morbidity in children with Type 1 diabetes mellitus. Around seven per thousand episodes of diabetic ketoacidosis (DKA) are complicated by cerebral oedema, and one-quarter of those children will die from it. The cause or causes of cerebral oedema are still very poorly understood, but lawyers are already keen to implicate various aspects of the management of DKA. There have been many theories as to the pathophysiology of cerebral oedema, and possible contributing factors may be excessive rate of rehydration, falling plasma osmolality (particularly that due to a reduction in plasma sodium concentration), hypoxia and insulin dosage. There is some supportive evidence for all of these factors in some cases, but there have been no sizeable case-control studies, in part because of the rarity of the condition. Furthermore, cerebral oedema can still occur even when the management of DKA follows current 'best practice' guidelines. As the mechanisms of cell volume regulation within the brain are increasingly understood, different questions may provide greater insights. For example, what is it about children that makes them so much more susceptible to cerebral oedema than adults? And why does one child treated in a certain way develop cerebral oedema whereas another does not? The anxiety over causing cerebral oedema has driven most of the changes in the management of DKA over recent decades, yet there is no evidence that the incidence has reduced. Until the causes are understood, we cannot be dogmatic about treatment recommendations.     

Postpartum blindness: two cases

We present 2 cases, one eclamptic patient and one noneclamptic patient, of headache, cortical blindness, and seizures. Both patients demonstrated findings consistent with posterior leukoencephalopathy syndrome. Posterior leukoencephalopathy syndrome is a rapidly evolving neurologic condition that is characterized by headache, nausea and vomiting, seizures, visual disturbances, altered sensorium, and occasionally focal neurologic deficits. Posterior leukoencephalopathy syndrome can be triggered by numerous conditions, including preeclampsia-eclampsia, and can be seen in the postpartum period. It is characterized predominately by white matter vasogenic edema of the occipital and posterior parietal lobes. This condition can be difficult to differentiate clinically from cerebral ischemia, and magnetic resonance imaging with diffusion-weighted imaging and apparent diffusion coefficient are needed to do so. In most cases of posterior leukoencephalopathy syndrome, the prognosis is excellent, with full resolution of symptoms.