Severe Hypernatremia Research Articles

Diabetes Insipidus after Traumatic Brain Injury.

Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI.

Severe hypercalcemia and hypernatremia in a patient treated with canagliflozin.

SummaryDrugs that inhibit the sodium-glucose co-transporter-2 (SGLT2) are an exciting novel, insulin-independent treatment for diabetes that block glucose reabsorption from the proximal tubules of the kidney, leading to increased glucose excretion and lower blood glucose levels. Inhibition of SGLT2 activity also reduces sodium reabsorption, which together with glycosuria produces a mild diuretic effect with the potential for dehydration and hyperkalemia. We report on a 60-year-old man with uncontrolled type 2 diabetes treated with insulin, glimepiride, metformin and canagliflozin, who was admitted with altered mental status after a syncopal episode. He had a 1-week history of ingestion of Tums for heartburn followed by poor appetite and lethargy. Laboratory work-up showed acute kidney injury, diabetic ketoacidosis (DKA), and parathyroid hormone-independent severe hypercalcemia of 17.4 mg/dl. DKA resolved with insulin treatment, and saline hydration led to improvement in hypercalcemia and renal function over 48 h, but was accompanied by a rapid increase in the serum sodium concentration from 129 to 162 mmol/l despite changing fluids to 0.45% saline. Urine studies were consistent with osmotic diuresis. Hypernatremia was slowly corrected with hypotonic fluids, with improvement in his mental status over the next 2 days. This is the first report of hypercalcemia associated with the use of a SLGT2 inhibitor. Although the exact mechanism is unknown, canagliflozin may predispose to hypercalcemia in patients ingesting excessive calcium because of dehydration from osmotic diuresis, with reduced calcium excretion and possible increased intestinal calcium absorption. Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss.Learning points Canagliflozin, an SGLT2 inhibitor, may cause hypercalcemia in susceptible patients.Although the exact mechanisms are unknown, dehydration from osmotic diuresis and increased intestinal calcium absorption play a role.Close monitoring of serum calcium levels is recommended in patients treated with SGLT2 inhibitors who are elderly, have established hypercalcemia, or take oral calcium supplements.Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss in susceptible patients.

Predialysis hypernatremia is a prognostic marker in acute kidney injury in need of renal replacement therapy

Background and ObjectivesThe present study aimed to evaluate the prognostic impact of predialysis dysnatremia in patients with acute kidney injury requiring renal replacement therapy (RRT). Design, Setting, Participants, and MeasurementsA secondary analysis of a prospective multicenter cohort study was performed. Serum sodium (Na) concentrations were categorized immediately before the first RRT as normonatremia (135≤Na ≤145mEq/L), hyponatremia (mild [130≤Na ≤134mEq/L] or severe [Na ≤129mEq/L]), and hypernatremia (mild [146≤Na ≤155mEq/L] or severe [Na ≥156mEq/L]). Multivariable logistic regression was used to estimate the impact of sodium levels categories on hospital mortality. ResultsDysnatremia occurred in 47.3% of 772 included patients. Hypernatremia was more frequent than hyponatremia (33.7% vs 13.6%, P=.001). Intensive care unit (ICU) and hospital mortality rates were 64.6% and 69%, respectively. Hospital mortality was higher in severe hypernatremia (89.1% [95% confidence interval {CI}, 78.7%-95.8%] vs 64.6% [CI, 59.8%-69.2%], P<.001, in normonatremia). Older patients, clinical admission, number of comorbidities, length of ICU stay before the beginning of RRT, and the number of organ dysfunctions were associated with higher hospital mortality. In multivariate analysis, severe hypernatremia (odds ratio, 2.87; 95% CI, 1.2-6.9), poor chronic heath status, severity of illness, sepsis, and lactate were independently associated with outcome. ConclusionAlmost 50% of patients with acute kidney injury in need of RRT in the ICU had mild or severe dysnatremia before dialysis initiation. Hypernatremia was the main sodium disturbance and independently associated with poor outcome in the study population.

Incidence, severity and prognosis associated with hypernatremia in dogs and cats.

BackgroundHypernatremia has been associated with substantial morbidity and death in human patients. The incidence and importance of hypernatremia in dogs and cats has not been determined.Hypothesis/ObjectivesTo describe the incidence of and prognosis associated with hypernatremia in dogs and cats at a university teaching hospital.AnimalsA total of 16,691 dogs and 4,211 cats with measured blood or serum sodium concentration.Methods Retrospective study. Medical records of animals with a blood or serum sodium concentration measured during a 60‐month period were reviewed to determine the severity of hypernatremia and its associated case fatality rate. Cases with moderate (11–15 mmol/L above the reference range) or severe hypernatremia (≥16 mmol/L above the reference range) were further reviewed.ResultsA total of 957 dogs (5.7%) and 338 cats (8.0%) were diagnosed with hypernatremia. Case fatality rates of dogs and cats with hypernatremia was 20.6 and 28.1%, respectively compared to 4.4 and 4.5% with a normal blood or serum sodium concentration (P < .0001). The magnitude of hypernatremia was linearly associated with a higher case fatality rate (P < .0001). Hypernatremia was associated with a higher case fatality rate than hyponatremia. Among the animals with moderate or severe hypernatremia, 50% of dogs and 38.5% of cats presented with community‐acquired hypernatremia, and 50% of dogs and 61.5% of cats developed hospital‐acquired hypernatremia.Conclusions and clinical importanceHypernatremia was found infrequently in this population but was associated with increased case fatality rates in dogs and cats. Presence and severity of hypernatremia might be useful as a prognostic indicator.

Novel mutations associated with nephrogenic diabetes insipidus. A clinical-genetic study.

Molecular diagnosis is a useful diagnostic tool in primary nephrogenic diabetes insipidus (NDI), an inherited disease characterized by renal inability to concentrate urine. The AVPR2 and AQP2 genes were screened for mutations in a cohort of 25 patients with clinical diagnosis of NDI. Patients presented with dehydration, polyuria-polydipsia, failure to thrive (mean ± SD; Z-height -1.9 ± 2.1 and Z-weight -2.4 ± 1.7), severe hypernatremia (mean ± SD; Na 150 ± 10 mEq/L), increased plasma osmolality (mean ± SD; 311 ± 18 mOsm/Kg), but normal glomerular filtration rate. Genetic diagnosis revealed that 24 male patients were hemizygous for 17 different putative disease-causing mutations in the AVPR2 gene (each one in a different family). Of those, nine had not been previously reported, and eight were recurrent. Moreover, we found those same AVPR2 changes in 12 relatives who were heterozygous carriers. Further, in one female patient, AVPR2 gene study turned out to be negative and she was found to be homozygous for the novel AQP2 p.Ala86Val alteration. Genetic analysis presumably confirmed the diagnosis of nephrogenic diabetes insipidus in every patient of the studied cohort. We emphasize that we detected a high presence (50 %) of heterozygous females with clinical NDI symptoms. • In most cases (90 %), inherited nephrogenic diabetes insipidus (NDI) is an X-linked disease, caused by mutations in the AVPR2 gene. • In rare occasions (10 %), it is caused by mutations in the AQP2 gene. What is new: • In this study, we report 10 novel mutations associated with NDI. • We have detected a high presence (50 %) of heterozygous carriers with clinical NDI symptoms.

Netherton Syndrome in a Neonate with Possible Growth Hormone Deficiency and Transient Hyperaldosteronism.

Netherton syndrome, a rare autosomal recessive genetic disorder, is classified as an ichthyosiform syndrome. In this report we present the case of a neonate with erythroderma shortly after birth, accompanied by severe hypernatremia, recurrent infections, transient hyperaldosteronism, and signs of growth hormone (GH) deficiency. DNA molecular analysis in the SPINK5 gene revealed heterozygosity in our index patient for 238insG and 2468delA frameshift mutations in exons 4 and 26, respectively, in the maternal allele and 1431-12G>A splice-site mutation in intron 15 in the paternal allele as well as the missense variation E420K in homozygous state. Combination of the identified mutations along with transient hyperaldosteronism and possible GH deficiency have not been described before. Accordingly, the importance of early multidisciplinary approach is highlighted, in order to reach accurate diagnosis, initiate prompt treatment, and ensure survival with fewer disease complications.

A Rare Case of Type II Autoimmune Hepatitis

Introduction: While type I autoimmune hepatitis (AIH) is widely studied in all demographics, type II AIH is far less common and classically occurs in female children. While rare in adults, it can initially present as fulminant hepatitis. Early consideration of this diagnosis is paramount in the prevention of poor outcomes. An 18-year-old female was referred for evaluation of painless jaundice. On initial presentation, she was 8 months post-partum after an uncomplicated vaginal delivery and had no other medical history. She first noted jaundice 5 days prior to presentation. Review of systems was otherwise negative. She denied history of drug, alcohol, or acetaminophen use. Her only medication was etonogestrel, a hormone-releasing implant, placed 6 months prior. Laboratory values showed a total bilirubin of 15.6, AST-1099, ALT-942, and Alk Phos-218. CT of the abdomen was significant only for calcified granulomas in the liver of unclear etiology. Initial viral and autoimmune work-up was negative, as was testing for Wilson’s and hemochromatosis. She underwent transjugular liver biopsy that revealed massive panlobular/panacinar necrosis involving 70% of the parenchyma with interface hepatitis, consistent with fulminant hepatitis. Possible etiologies included autoimmune, viral, druginduced, and Wilson’s. Further staining revealed no evidence of iron or copper. The patient underwent extensive serologic testing. Over the next several days, she had progressive declining of liver function, with worsening coagulopathy and the development of encephalopathy. She was started empirically on steroids for AIH. Given worsening mental status, she had an ICP monitor placed and was listed status 1A for transplant. Cerebral edema continued to increase and an organ offer became available. The patient underwent emergent liver transplantation. Post-operatively, she had persistently elevated ICP, and continued to require pentobarbital and hyperosmolar therapy. She developed severe hypernatremia as high as 195, necessitating termination of hyperosmolar therapy. On post-op day 5, she was taken to the OR for closure of the abdomen. That night, she rapidly declined, at which time she was found to have severe anion-gap acidosis, possibly related to sepsis and propylene glycol toxicity. She became unstable and required pressor support, and deteriorated before CVVH could be initiated. She suffered a PEA arrest and passed. Pathologic evaluation of her native liver re-demonstrated findings detailed in the initial biopsy. Anti-LKM AB was positive. This case of an 18-year-old female with type 2 AIH that was rapidly progressive underlies the importance of early recognition and empiric treatment to avoid life-threatening complications.

Hypernatrémie majeure par intoxication à l’eau de mer chez un enfant

Drowning in sea water is an unusual cause of severe hypernatremia. We report the case of a 3.5-year-old boy who died 11h after drowning in sea water, with a serum sodium level of 178 mmoL/L. In this case, hypernatremia was aggravated by diarrhea and hyperglycemia with glycosuria. Usually, correction of acute hypernatremia must be quick and early, aiming at a reduction of serum sodium concentration of up to 1-2 mmoL per liter per hour.

Prevalence of severe hypokalaemia in patients with traumatic brain injury

IntroductionPatients with traumatic brain injury (TBI) are more vulnerable to develop hypokalaemia, we sought to investigate the prevalence, and the relationship between severe hypokalaemia and the mortality of traumatic brain injury patients. MethodsIsolated traumatic brain patients who had hypokalaemia (serum potassium <3.5mmol/L) and age≥14yrs were recruited into the study between January 2008 and March 2013. Hypokalaemia was defined as potassium level in the blood <3.5mmol/L during the hospitalisation, which was classified by severity: mild (3.0mmol/L≤K<3.5mmol/L), moderate (2.5mmol/L≤K<3.0mmol/L) and severe (K<2.5mmol/L). Multivariable logistic regression was performed to find the impact of hypokalaemia on mortality. ResultsA total 375 cases were included in analysis. The peak incidence of severe hypokalaemia occurred in the first 24–96h. TBI patients with severe hypokalaemia had significantly higher serum sodium and lower serum phosphorus than those patients with mild or moderate hypokalaemia (p<0.001). Compare to other groups, the severe hypokalaemia group had the worst outcome. Moreover, the patients (n=15) who had severe hypokalaemia, hypernatraemia (Na>160mmol/L), and hypophosphataemia (P<0.3mmol/L) all died in hospital. Multiple logistic regression analysis resulted in decrease of GCS (OR=1.27; 95% CI=1.15–1.41; p<0.001) and potassium (OR=4.35; 95% CI=2.04–9.26; p<0.001) being associated with significant increased risk of mortality. ConclusionsThe peak incidence of severe hypokalaemia occurred in the first 24–96h. TBI patients with severe hypokalaemia are more vulnerable to develop hypophosphataemia and hypernatraemia than patients with mild and moderate hypokalaemia. Severe hypokalaemia are the independent risk factors for mortality in TBI patients.

Severe Hyperthermia, Hypernatremia, and Early Postoperative Death After Transethmoidal Cavitron Ultrasonic Surgical Aspirator (CUSA)‐Assisted Diencephalic Mass Removal in 4 Dogs and 2 Cats

To report clinical findings including severe hyperthermia and hypernatremia after transethmoidal Cavitron ultrasonic surgical aspirator (CUSA)-assisted diencephalic mass removal. Retrospective case series. Dogs (n = 4) and 2 cats. Medical records (1997-2003) of dogs and cats that had transethmoidal CUSA-assisted diencephalic mass removal were reviewed. Retrieved data were: history, signalment, blood work, neurologic examination findings, MRI results, histopathology, postoperative complications, pre- and postoperative medical therapy, and outcome. Tumor types included: meningioma (n = 3), choroid plexus papilloma (1), astrocytoma (1), and pituitary macroadenoma (1). Median onset of hyperthermia was 3.5 hours (range: 1-6 hours) after extubation; median high temperature at onset was 40.3°C, (range: 39.6-41.7°C). Median onset of hypernatremia (median, 172 mmol/L; range: 168-196 mmol/L) was 4.5 hours (range: 1-9 hours) after extubation. Median time of death after hyperthermia was 10.5 hours (range: 6-13 hours) and after extubation was 13.5 hours (range: 11-15 hours). Transethmoidal CUSA-assisted diencephalic mass removal is associated with early postoperative hyperthermia, hypernatremia, and death, and cannot be recommended.

Undercorrection of hypernatremia is frequent and associated with mortality

BackgroundAbout 1% of patients admitted to the Emergency Department (ED) have hypernatremia, a condition associated with a mortality rate of 20 to 60%. Management recommendations originate from intensive care unit studies, in which patients and medical diseases differ from those in ED.MethodsWe retrospectively studied clinical characteristics, treatments, and outcomes of severely hypernatremic patients in the ED and risk factors associated with death occurrence during hospitalization.ResultsDuring 2010, 85 cases of severe hypernatremia ≥150 mmol/l were admitted to ED. Hypernatremia occurred in frail patients: mean age 79.7 years, 55% institutionalized, 28% with dementia.Twenty four percent of patients died during hospitalization. Male gender and low mean blood pressure (MBP) were independently associated with death, as well as slow natremia correction speed, but not the severity of hyperosmolarity at admission. Infusion solute was inappropriate for 45% of patients with MBP <70 mmHg who received hypotonic solutes and 22% of patients with MBP ≥70 mmHg who received isotonic solutes or were not perfused.ConclusionsThis is the first study assessing outcome of hypernatremic patients in the ED according to the treatment provided. It appears that not only a too quick, but also a too slow correction speed is associated with an increased risk of death regardless of initial natremia. Medical management of hypernatremic patients must be improved regarding evaluation and treatment.

Hypernatremia: correction rate and hemodialysis.

Severe hypernatremia is defined as serum sodium levels above 152 mEq/L, with a mortality rate ≥60%. 85-year-old gentleman was brought to the emergency room with altered level of consciousness after refusing to eat for a week at a skilled nursing facility. On admission patient was nonverbal with stable vital signs and was responsive only to painful stimuli. Laboratory evaluation was significant for serum sodium of 188 mmol/L and water deficit of 12.0 L. Patient was admitted to medicine intensive care unit and after inadequate response to suboptimal fluid repletion, hemodialysis was used to correct hypernatremia. Within the first fourteen hours, sodium concentration only changed 1 mEq/L with a fluid repletion; however, the concentration dropped greater than 20 mEq/L within two hours during hemodialysis. Despite such a drastic drop in sodium concentration, patient did not develop any neurological sequela and was at baseline mental status at the time of discharge.

Could neonatal hypernatremia dehydration influence hearing status?

Neonatal hypernatremia dehydration (NHD) is a dangerous condition in neonates, which is accompanied by acute complications (renal failure, cerebral edema, and cerebral hemorrhage) and chronic complications (developmental delay). Children begin learning language from birth, and hearing impairment interferes with this process. We assessed the hearing status of infants with hypernatremia dehydration. In a case-control study in 110 infants presenting at the Ghaem Hospital (Mashhad, Iran) between 2007 and 2011, we examined the incidence of hearing impairment in infants suffering from hypernatremia dehydration (serum sodium >150 mEq/L) in comparison with infants with normal sodium level (serum sodium ≤150 mEq/L). Three of 110 cases examined in the study group showed a transient hearing impairment. A mean serum sodium level of 173mg/dl was reported among hearing-impaired infants. Transient hearing impairment was higher in infants with hypernatremia; although this difference was not significant (P>0.05). Hearing impairment was observed in cases of severe hypernatremia.

Sodium lactate for fluid resuscitation: the preferred solution for the coming decades?

In a recent issue of Critical Care, 0.5 M sodium lactate infusion for 24 hours was reported to increase cardiac output in patients with acute heart failure. This effect was associated with a concomitant metabolic alkalosis and a negative water balance. Growing data strongly support the role of lactate as a preferential oxidizable substrate to supply energy metabolism leading to improved organ function (heart and brain especially) in ischemic conditions. Due to its sodium/chloride imbalance, this solution prevents hyperchloremic acidosis and limits fluid overload despite the obligatory high sodium load. Sodium lactate solution therefore shows many advantages and appears a very promising means for resuscitation of critically ill patients. Further studies are needed to establish the most appropriate dose and indications for sodium lactate infusion in order to prevent the occurrence of severe hypernatremia and metabolic alkalosis.

Evaporation of free water causes concentrational alkalosis in vitro

The development of metabolic alkalosis was described recently in patients with hypernatremia. However, the causes for this remain unknown. The current study serves to clarify whether metabolic alkalosis develops in vitro after removal of free water from plasma and whether this can be predicted by a mathematical model. Ten serum samples of healthy humans were dehydrated by 29 % by vacuum centrifugation corresponding to an increase of the contained concentrations by 41 %. Constant partial pressure of carbon dioxide at 40mmHg was simulated by mathematical correction of pH [pH(40)]. Metabolic acid-base state was assessed by Gilfix' base excess subsets. Changes of acid-base state were predicted by the physical-chemical model according to Watson. Evaporation increased serum sodium from 141 (140-142) to 200 (197-203) mmol/L, i.e., severe hypernatremia developed. Acid-base analyses before and after serum concentration showed metabolic alkalosis with alkalemia: pH(40): 7.43 (7.41 to 7.45) vs 7.53 (7.51 to 7.55), p = 0.0051; base excess: 1.9 (0.7 to 3.6) vs 10.0 (8.2 to 11.8), p = 0.0051; base excess of free water: 0.0 (- 0.2 to 0.3) vs 17.7 (16.8 to 18.6), p = 0.0051. The acidifying effects of evaporation, including hyperalbuminemic acidosis, were beneath the alkalinizing ones. Measured and predicted acid-base changes due to serum evaporation agreed well. Evaporation of water from serum causes concentrational alkalosis in vitro, with good agreement between measured and predicted acid-base values. At least part of the metabolic alkalosis accompanying hypernatremia is independent of renal function.

Severe hypernatremia and hyperchloremia in an elderly patient with IgG-kappa type

Severe hypernatremia and hyperchloremia in an elderly patient with IgG-kappa type Kenrick BerendSt Elisabeth Hospital, Willemstad, Cura&ccedil;aoImashuku et al1 describe a 77-year-old male patient with multiple myeloma who was admitted to the hospital after suffering a pelvic bone fracture due to a road traffic accident. Several days after admission the arterial blood gas showed a pH of 7.481; arterial carbon dioxide tension (PaCO2) of 28.2 mmHg; arterial oxygen tension (PaO2) of 84.0 mmHg; HCO3- of 20.8 mmol/L (normal; 23&ndash;31 mmol/L); and an anion gap of 8.9 mmol/L (normal;12 mmol/L). These data, as the authors concluded, were suggestive of metabolic acidosis. First, this is not true because a high pH and low PaCO2 confirm a respiratory alkalosis. Since the test was conducted days later we may expect a chronic respiratory alkalosis to be present, perhaps because of pain or a secondary pulmonary problem, as may be expected with a relatively low PaO2. In chronic respiratory alkalosis one would expect the HCO3- to decrease about 4 mmol/L with every 10 mmHg decrease of PaCO2.2 If the initial HCO3- had been about 25 mmol/L, the expected PaCO2 would be about 20.28 mmol/L, almost identical with the patient&rsquo;s HCO3-.View original paper by Imashuku and colleagues.

Transient diabetes insipidus with severe maternal and fetal hypernatremia

Abstract Diabetes insipidus is a condition characterised by polyuria and polydipsia with excretion of diluted urine. Transient diabetes insipidus has been reported in pregnancy and is often associated with acute fatty liver of pregnancy, pre-eclampsia, HELLP syndrome and multiple pregnancy. Presenting symptoms can be vague. In our case, a primigravida with spontaneous monochorionic diamniotic twin pregnancy presented at 36+3 weeks in early labour. Severe hypernatremia was found in the patient and in both twins after a caesarean section was performed. Transient diabetes insipidus was diagnosed based on paired serum and urine osmolality. The hypernatremia was corrected gradually and 1-deamino-8D-arginine vasopressin was given. A high index of suspicion and early involvement of physicians and paediatricians are needed to avoid catastrophic consequences.

Adipsia and hypernatraemia in a 6-month-old Staffordshire bull terrier

A 6-month-old female Staffordshire bull terrier cross presented to the Onderstepoort Veterinary Academic Hospital with lethargy, weakness, decreased appetite, abnormal vocalisation, twitching of the facial muscles and ears, circling, alopecia, pruritus, seborrhoea sicca and erythema. Serum biochemistry revealed severe hypernatraemia (200.4 mmol/L; Reference Interval 140 mmol/L – 155 mmol/L). Treatment required careful administration of intravenous fluids. The electrolytes were monitored to ensure slow and controlled sodium normalisation (the target reduction of Na concentration was by 0.5 mmol/L/h –1 mmol/L/h or 12 mmol/L/24 h – 24 mmol/L/24 h). Despite the careful fluid calculations and close monitoring, the serum sodium levels dropped more than the recommended 0.5 mmol/L/h – 1 mmol/L/h in the first 4 h and the fluids had to be adjusted. The patient’s habitus improved and the central nervous system signs started to resolve after 1 day of fluid treatment. The puppy started eating food mixed with water, but made no attempt to drink water. The pruritus and erythema resolved once the sodium levels normalised and the seborrhoea sicca began to resolve. At a follow up visit 20 days post discharge the skin was normal. A diagnosis of hypernatraemia as a result of pure water loss due to hypodipsia or adipsia was made, as the puppy made no attempt to drink water when her serum sodium levels increased (a strong thirst stimulus). Hypernatraemia recurred if she was not forced to take in adequate amounts of water mixed with her food. Dermatological changes such as seborrhoea, hyperkeratosis and alopecia have been reported in a few other cases of hypernatraemia in dogs and sodium levels should be investigated in dermatological patients when no other cause can be established. This study, supported by another retrospective study done in 2008, suggests that the Staffordshire bull terrier may be a breed that is predisposed to hypernatraemia.

Hypoglycaemia at point of hospital admission of under-five children with acute diarrhoea: Prevalence and risk factors

Background: Hypoglycaemia is one of life-threatening immediate complications of acute diarrhoea among under-five children but its diagnosis may be overlooked because all the symptoms may be mimicked by severe dehydration.Objective: To determine the prevalence of hypoglycaemia at the point of hospital admission of under-five children with acute diarrhoea and identify some of the risk factors.Methods: At the point of hospital admission, venous blood sample was collected into an appropriate sample bottle (fluoride-oxalate bottle) from 201 under-five children with acute diarrhoea for blood glucose determination. The blood samples were analysed using the glucose-oxidase method. One of the authors administered a questionnaire to each of the caregiver to obtain information on the socio-demographic characteristics and the clinical profile (e.g., presence or absence of vomiting, duration of acute diarrhoea, time of last meal of the patients, and administration of ORS at home. Hypoglycaemia was defined asblood glucose value below 2.6 mmol/L.Results: At the point of hospital admission, 7.7% (14 of 183; CI =3.7-11.7) under-five children with acute diarrhoea had hypoglycaemia(blood glucose &lt; 2.6 mmol/L) but dropped to 4.9% (CI=2.9-6.9)when a cutoff point of &lt; 2.2 mmol/L was applied. The risk factors forhypoglycaemia were the presence of severe dehydration (p&lt;0.001),hypernatraemia and acidosis (p&lt;0.001). The prevalence of hypoglycaemia was 7 times higher in children whose time of last meal was . 8 hours compared with their counterparts whose time of last meal was &lt; 8 hours. Mortality rate was significantly higher in children with acute diarrhoea and hypoglycaemia compared with their counterparts with normoglycaemia(p&lt;0.01).Conclusion: In acute diarrhea, hypoglycaemia is an important comorbidityamong children aged below 36 months and the significant associated risk factors for hypoglycaemia are severe dehydration, hypernatraemia andacidosis. Under-five children presenting with acute diarrhoea and hypoglycaemia at point of hospitalization are at a significantly greater risk of death.Key words: Acute diarrhoea, hypoglycaemia, hypernatraemia,

A not very essential obesity: the Rohhad Syndrome. Description of two cases and review of the literature

Rapid-onset Obesity with Hypothalamic Dysfunction, Hypoventilation, and Autonomic Dysregulation (ROHHAD) is a rare and complex pediatric disorder. Children typically show ROHHAD after the first years of life with rapid weight gain and subsequently autonomic nervous system dysregulation (altered pain perception, pupillary dysfunction, hypothermia and bradycardia); alveolar hypoventilation with risk of cardiorespiratory arrest and hypothalamic dysfunction (central diabetes insipidus, hypothyroidism, growth hormone and corticotrophin deficiency). Tumours of neural crest origin, such as ganglioneuroblastoma and ganglioneuronoma, are reported in 33% of the patients and may be found in the chest or abdomen. Here we describe two girls who presented with rapid weight gain, at the age of 5 and 9 years respectively. The first was admitted due to obesity and central hypothyroidism. After two months she rapidly developed a clinical picture characterized by thermal dysregulation, hypodipsia and severe hypernatriemia, hypertrigliceridemia, alveolar hypoventilation supported by mechanical ventilation. The second presented with rapid-onset obesity and a mild hyperprolactinemia. After three months of follow-up she was admitted due to a clinical picture of hypothermia, seizures and hyponatremia. Subsequentely she developed altered water balance (severe hypernatremia) and severe hypoventilation. Chest CT and MR imaging showed a posterior mediastinal mass. Endocrinological investigation showed corticotrophin deficiency and central hypothyroidism treated with specific replacement therapies. On the basis of our experiences we can infer that it is necessary perform specific further investigations of hypothalamic function in all the children with rapid onset obesity in order to early prevent the catastrophic consequences that may occur in this syndrome.