Severe Hypernatremic Dehydration Research Articles

Severe Hypernatremic Dehydration in a Neonate

Hypernatremia, a rare condition in newborns, is marked by elevated plasma sodium levels exceeding 150 mEq/L. It is more common in newborns who are exclusively breastfed or with excessive weight loss. Hypernatremic dehydration (HD) presents severe risks, including cerebral edema and other neurological complications. A female newborn, 12 days old (birth weight: 2800g), was brought to the Emergency Department due to a 30% decrease in birth weight and reduced urine output. The newborn was solely breastfed every 2 hours, with a good notion of adequate reflexes and tolerance. Physical examination revealed a skeletal appearance, jaundice, sunken eyes and skin turgor. Blood pressure measurement was unsuccessful, while capillary blood glucose was 96g/dL. A saline bolus (10 mL/Kg)was administered. Venous blood gas analysis showed pH 7.39, lactate 4.3 mmol/L, HCO3-21.8 mmol/L, and Na+ 180 mEq/L.

Refractory seizure in a neonate with severe hypernatraemic dehydration – A case report

Hypernatraemic dehydration is a common clinical condition seen in neonates especially when they lose weight by more than 10%. Such neonates should be carefully followed up for rising sodium levels and need to be encouraged adequate feeding to prevent complications. Term-appropriate neonate born to a non-consanguineous couple with an uneventful perinatal period was brought to the paediatric emergency room on day 15 of life with multiple seizures and was diagnosed with hypernatraemic dehydration. Her brain imaging demonstrated sagittal venous thrombosis with intraventricular haemorrhage and parenchymal bleeding with infarct. She was managed with respiratory support and fluid management. Parents were counselled regarding the guarded prognosis. She was discharged against medical advice.

An exhaustive battle of salt: A challenging case of Adipsic Diabetes Insipidus following resection of Craniopharyngioma

Introduction: Even though rare, Adipsic Diabetes Insipidus (ADI) is a potentially life-threatening complication of craniopharyngioma: due to the mass effect of the tumor or perioperative consequences leading to severe hypernatremic dehydration. Even in expert hands, management of water balance, in the absence of thirst is extremely challenging. Case Description: A 25-year-old gentleman, an electrician presented to the neurosurgical casualty with worsening headaches, impaired vision, and features of raised intracranial pressure over 2 months. He was found to have a large cystic suprasellar mass with well-defined margins measuring 2.7cm x 2.7cm x 3cm with chiasmal compression, suggestive of craniopharyngioma, complicating with bitemporal hemianopia, hypogonadotropic hypogonadism (LH 0.78IU/L, FSH 1.2IU/L, Testosterone 33ng/dL), secondary hypothyroidism, cranial diabetes insipidus, prediabetes sparing the cortisol axis. He underwent transcranial resection of the tumor, revealing WHO grade1 adamantinomatous craniopharyngioma followed by radiotherapy. The post-operative period was complicated with severe hypernatremia despite escalating doses and changing dosage forms of desmopressin from parenteral to nasal spray to oral tablets. Two weeks following discharge, he presented with severe hypernatremia (176mEq/L), polyuria, weight loss, hypotension, and altered sensorium where his lack of thirst was appreciated. Conclusions: In those with ADI, for the management of water balance, a “personalized approach” with the involvement of both patient and family is of paramount importance. With appropriate dose titration of desmopressin, careful fluid prescription, and frequent monitoring of electrolytes even at best centers, it is a battle that is hard to win.

Diffuse Miliaria Cristalina due to Severe Hypernatremic Dehydration: A Neonatal Case Report with a Current Literature Review

Diffuse Miliaria Cristalina due to Severe Hypernatremic Dehydration: A Neonatal Case Report with a Current Literature Review

Nasolabial and distal limbs dry gangrene in newborn due to hypernatremic dehydration with disseminated intravascular coagulation: a case report

IntroductionGangrene is the death of an organ or tissue due to lack of blood supply or bacterial infection. In neonates, gangrene is usually caused by sepsis, dehydration, maternal diabetes, asphyxia, or congenital anticoagulant deficiency. It commonly occurs in the extremities. Gangrene may lead to death or amputation of the limb. Early diagnosis and prompt management of the underlying cause halts the progression of the disease.Case presentationA 12-day-old neonate presented with a complaint of black discoloration of the nose and feet for 2 days. He was breastfeeding poorly and had signs of dehydration. Upon physical examination, he was tachycardic (pulse rate = 182 beats per minute), tachypneic (respiratory rate = 62 breaths per minute), and hypothermic (temperature = 35.0 oC). He lost 33.3% of his birth weight. He had demarcated cold, dry, and dark discoloration of the entire nose, nasal septum; upper lip; palate; bilateral distal lower limbs; and the left fifth finger. Dorsalis pedis arteries were not palpable on either side. On investigation, the baby had pancytopenia, hypernatremia, elevated creatinine, elevated coagulation profiles, and absent arterial flow in bilateral dorsal pedis arteries. He was treated for hypernatremic dehydration and possible sepsis. He was transfused with whole blood, platelets, and fresh frozen plasma, but finally, the patient passed away on the 7th day of admission.ConclusionThe entire nose, upper lip, soft and hard palate, symmetric lower limb, and fifth finger gangrene due to severe hypernatremic dehydration complicated by disseminated intravascular coagulation may occur in the same patient. To avoid such serious neonatal problems, mothers should be properly educated about optimal breastfeeding techniques and schedule well-child visits 3–5 days after birth.

Hipernatremi ve milarya kristalina: nadir bir ilişki

Miliaria crystallina is a common, transient and self-limited cutaneous disorder, caused by blockage within the eccrine sweat duct. Herein, we report a neonatal case with miliaria crystallina developed during treatment of severe hypernatremic dehydration. The effective treatment and prevention of miliaria crystallina is to avoid further sweating. On the basis of the presented patient, we consider that miliaria crystallina may be rarely developed in newborns with severe hypernatremia but this condition is transient and self-limited.

Management of severe hypernatremic dehydration and acute kidney injury in children in a critical care nephrology and dialysis unit.

Our study aimed to manage the children presented with severe hypernatremic dehydration and acute kidney injury (AKI) an updated fluid management protocol was used to find out the rate of decline of serum sodium per day and their outcome. This is a prospective interventional study was conducted from November 2015 up to October 2016 in the Critical Care Nephrology and Dialysis Unit of Dhaka Shishu (Children) Hospital, Bangladesh. A total of 45 children with hypernatremia and AKI were evaluated. Patients were treated by the calculated amount of dextrose in normal saline mixed with various dilutions of 3% NaCl with a difference of serum to infusate sodium concentration around 10 mEq/L as per the American Academy of Pediatrics - 2005. Intermittent peritoneal dialysis was done when in the failure stage of AKI or when serum sodium (Na+) >180 mEq/L. Depending on the outcome samples were divided into survival and death groups. Data were processed by software STATA 13 and analysis was done by one-way ANOVA, Tukey test, Chi-square test, F-test, and Student's t-test. Age ranged from one month to 6½ years and 91% were infants. Total 64% of patients were in the failure stage of AKI and majority were in the death group, 31% in injury and 4.4% patient in the risk stage. Out of 45 cases, 30 (67%) had severe hypernatremia. Significant reduction of serum Na+ was found and the rate of decline between days was optimum (8.4 mmol/L/day). Overall 60% survived with normal renal functions and 40% died. The calculated amount of dextrose in normal saline mixed with various dilutions of 3% NaCl is safe in severe hypernatremic dehydration with AKI.

A Case of Congenital Glucose Galactose Malabsorption with a New Mutation in the SLC5A1 Gene

Congenital glucose-galactose malabsorption (CGGM) is an autosomal recessive disorder originating from an abnormal transporter mechanism in the intestines. It was sourced from a mutation in the SLC5A1 gene, which encodes a sodium-dependent glucose transporter. Here we report a 2-day-old girl with CGGM who presented with severe hypernatremic dehydration due to diarrhea beginning in the first hours of life. Mutation analysis revealed a novel homozygous mutation NM_000343.3 c.127G > A (p.Gly43Arg) in the SLC5A1 gene. Since CGGM can cause fatal diarrhea in the early neonatal period, timely diagnosis of the disease seems to be essential.

SUN-277 Severe Hyperglycemia in the Setting of Hypernatremic Dehydration

Background: Hypernatremic dehydration associated with hyperglycemia in non-diabetic infants has a potential to cause serious metabolic derangement. Review of limited literature available on this condition reveals pathogenesis of hyperglycemia is likely multi-factorial. We present a case of extreme hyperglycemia in a 10 months old infant with severe hypernatremic dehydration with possible mechanisms discussed. Case Report: Our patient was a 10 months old Caucasian male former 25 weeks premature infant (birth weight: 0.79 kg) with chronic lung disease on furosemide and potassium supplements (KCl) presenting with lethargy, respiratory failure, severe hypovolemic shock and acute kidney injury (AKI) requiring intubation and aggressive fluid resuscitation with pressor support. Initial labs showed blood glucose (BG)> 750 mg/dl, repeat BG 1438 mg/dl, pH 7.09, PCO2 80 mm Hg, sodium 194 mmol/L, BUN 197 mg/dl, Cr 2.6 mg/dl, potassium 11 mmol/L, chloride 155 mmol/L, bicarb 22 mmol/L, POC ketones 4.7 mmol/L, beta hydroxybutyrate 0.58 mmol/L. Possibility of diabetic ketoacidosis was considered. Regular insulin drip was started at 0.05 units/kg/hour. Glucose levels normalized after approximately 17 hours. He remained euglycemic off insulin for rest of hospitalization on glucose containing fluids. C-peptide 17.99 ng/ml indicated endogenous insulin production. HbA1C was 6.2% with negative pancreatic autoantibodies. Associated risk factors were identified to include viral URI, 1 week of watery diarrhea and potential administration of inappropriately diluted (increased solute) formula and/or KCl overdose. Septic work up was negative. Hypernatremia slowly corrected over 10 days. AKI resolved and patient had no metabolic abnormalities prior to discharge. Conclusion: Hypernatremic dehydration is associated with significant morbidity and mortality and requires carefully controlled rehydration due to risk of cerebral edema. Hyperglycemia in such cases is typically transient, associated with normal insulin/C-peptide levels, negative pancreatic autoantibodies and often resolves with fluid resuscitation alone. However, extreme hyperglycemia as in our case may warrant initiation of insulin. The pathogenesis is unclear but related to a combination of insulin resistance induced by counter-regulatory hormones like cortisol, glucagon and growth hormone with increased endogenous glucose production and decreased peripheral glucose utilization. This may be compounded by altered renal glucose threshold in sick infants.

Inadequate Breastfeeding may lead to Severe Hypernatremia: A Case Report

Background: The benefits of breast feeding are well established worldwide. Inadequate breastfeeding may result in severe complications such as hypernatremic dehydration. This condition is rare and not well known. In this case report, we describe a case of severe hypernatremic dehydration revealed by fever with delayed consultation. Presentation of case: We report the case of an exclusively breastfed male newborn. He was referred on the 13th day of life because of lethargy and fever. He had a severe dehydration on clinical examination. Serum sodium was of 172 mmol/L. The breast milk sodium was high as compared to a volunteer control (85 mmol/L vs 19 mmol/L). Breastfeeding was temporarily suspended and reintroduced after 5 days with favorable evolution. Conclusion: Breast feeding associated hypernatremia can cause life-threatening complications in newborns. Prevention requires frequent and sufficient breastfeeding and weight gain monitoring during the first days of life.

Severe hypernatremic dehydration leading to bilateral lower limb ischemia in a neonate

No abstract available

Severe Hypernatraemic Dehydration and Unconsciousness in a Care-Dependent Inpatient Treated with Empagliflozin.

A 66-year-old Caucasian male became unconscious 2 weeks after initiation of add-on therapy with empagliflozin for poorly controlled type 2 diabetes mellitus. The inpatient had recently suffered focal pontine stroke, rendering him bedridden and requiring increased nursing care, including assistance with drinking. The patient had received empagliflozin 10 mg once daily for glycaemic control. Investigations revealed hypernatraemia (164 mmol/l), a urine glucose level of 3935 mg/dl, and a creatinine level of 2.1 mg/dl. The patient was diagnosed with severe hypernatraemic dehydration due to iatrogenic glucosuria and prerenal kidney failure. Empagliflozin was discontinued and the patient received hypotonic fluids (including 5% dextrose and free water). Over the following 4 days, glucosuria subsided, blood sodium levels and kidney function normalized and the patient regained full consciousness. He was discharged for rehabilitation 40 days after admission. A Naranjo assessment score of 6 was obtained, indicating a probable relationship between the patient’s hypernatraemic dehydration and administration of empagliflozin. In this care-dependent inpatient, who lost the ability to replace water loss autonomously because of a stroke, continuous administration of empagliflozin caused persistent glucosuria and contributed to progressive volume depletion. Excessive dehydration resulted from ignorance of both the populations that are susceptible to dehydration under sodium-glucose cotransporter 2 (SGLT2) inhibitor therapy and the drug’s mechanism of action. In patients who depend on support from others in daily tasks, including fluid intake, patients with an impaired sense of thirst and those who have lost the ability to communicate thirst, SGLT2 inhibitor therapy should not be initiated or might be (temporarily) discontinued.

Severe hypernatremic dehydration in a breastfed infant

Objective - To report a rare case of hypernatremic dehydration in an exclusively breastfed infant. Case report - We present a term newborn, 14-day-old boy, exclusively breastfed, who was lethargic and severely dehydrated upon admission (35% birth weight loss). The newborn was found to have severe hypernatremic dehydration (Na+ 197 mmol/l), acute renal insufficiency (Creatinine 273 umol/l) and metabolic acidosis. Also, the blood culture result was positive. Intravenous rehydration and antibiotic therapy were started. After 22 days of hospitalization, the infant was discharged home in a good general condition. Now the child is 13 months old, he is healthy and no neurologic sequelae are noticed. Conclusion - Hypernatremic dehydration in newborns is a rare complication, which is dangerous, but also preventable. Prevention consists in educating mothers about successful breastfeeding techniques, and also early newborn reassessment after discharge from the hospital is mandatory.

Widespread Miliaria Crystallina in a Newborn with Hypernatremic Dehydration

Miliaria, which is extravasation of sweat into the epidermis and dermis due to sweat duct obstruction, is a commonly seen dermatologic disorder in newborns. We present a case of extensive, widespread miliaria crystallina that developed in a newborn during treatment of severe hypernatremic dehydration. A possible mechanism could be the destruction of sweat ducts with excretion of sweat with high levels of sodium.

Life-Threatening Hypernatremic Dehydration in a 7-Week-Old Exclusively Breastfed Infant as a Cause of a Decline in Breastmilk Volume and Parental Language Barriers in a North African Family

Breast-feeding is regarded as the most appropriate source of nutrition for healthy, full-term newborns and infants. Here, we present the case of a full-term, seven week old male infant who was exclusively breast-fed but who developed severe hypernatremic dehydration as a result of declined breast milk volume that was not recognized by the parents. In order to prevent serious therapy-associated side effects due to rapid rehydration, we performed a rehydration regime providing a slow decrease of serum sodium levels by carefully infusing hypertonic saline solution. Following this approach, the patient could be discharged without any noticeable disorder. As the incidence of breast-feeding associated hypernatremic dehydration in the developed countries is increasing, strategies of prevention are discussed.

Clinical characterization of a girl with trisomy 20q13.2qter and monosomy 13q33.1qter: Delineating phenotype–genotype correlations

Array comparative genomic hybridization (aCGH) is a techniqueenabling high-resolution, genome-wide screeningof genomic seg-mentalcopynumbervariations(CNVs)[Solinas-Toldoetal.,1997;Pinkeletal.,1998].Itisbecominganessentialandaroutineclinicaldiagnostic tool and is gradually replacing cytogenetic methods.Most of the clinically available aCGH platforms are designed todetectaneuploidies,well-characterizedmicrodeletion/microdupli-cation syndromes and subtelomeric or other unbalanced chromo-somal rearrangements [Ballif et al., 2006; Shinawi and Cheung,2008]. The aim of the present paper is to present the clinical andmolecular description of a patient with a submicroscopic rear-rangement resulting in trisomy 20q and monosomy 13q andtherebytodelineatethephenotypeassociatedtoaspecificchromo-somal region.Thepatient,a6-year-oldgirl,istheproductofthefirstpregnancyofhealthy,nonconsanguineousparents,aged45years(mother)and51 years (father). The pregnancy was complicated by reduced fetalmovement and vaginal infection.Intrauterine diagnosis at the 7th month of pregnancy showedhypoplasia of the corpus callosum during the final month severeIUGR was diagnosed.Thepatientwasdeliveredat38weeksgestationviainducedlabor.The weight was 1,400g (<10th centile), length 45.5cm (10thcentile), and the OFC was 30cm (3rd centile). Examinationsimmediately after birth revealed that the patient had hyporeflexia,hypoactivity, and flattened occiput. The cerebral ultrasoundshowedthatshehadhypogenesisofthecorpuscallosum.Echocar-diographyand subsequent cardiac catheterization showed an osti-um secundum atrial septal defect and branch pulmonary stenosis.Congenital tracheal stenosis was diagnosed by a bronchoscopy.Fundus and evoked potentials were both normal.Significant psychomotor developmental delay was observed ininfancyandattheageof6years,shewasstillunabletostandalone.Vocalizations began at 4 years and at 6 years she said disyllabicnon-referentialwordsandcommunicatedwithsimplegestures.Shehad no developmental regression Since 3 years of age, she hasexperiencedsporadicseizures(5or6episodes)andreceivedfurthertreatment with valproic acid or clonazepam. No deterioration wasseeninassociationwiththeepisodes.Shehadslowweightgainandlongitudinal growth.Amongtheillnesshad,shewasadmittedat22monthsoldduetoan episode of acute gastroenteritis with severe hypernatremicdehydration and prerenal acute renal failure. In addition, she hashad several urinary tract infections with normal renal findings onsonogram.

Subclinical Venous Sinus Thrombosis Secondary to Hypernatraemic Dehydration

An 8-day-old infant was admitted to a paediatric intensive care unit with severe hypernatraemic dehydration. An MRI brain was performed which revealed extensive venous sinus thromboses. This is a recognised but rare complication of hypernatraemic dehydration and the importance of early detection and intervention of this condition is again highlighted.This is the first case report of venous sinus thrombosis secondary to hypernatraemic dehydration in a patient with no clinical neurological signs. We postulate that there may be a cohort of infants with subclinical cerebral venous thrombosis secondary to hypernatraemic dehydration.

Reducing the incidence of neonatal hypernatraemic dehydration

Iyer et al 1 report the effects of a neonatal weight-monitoring policy on the incidence of hypernatraemic dehydration. This policy led to an increased recognition of affected infants, and identified...

Hypernatraemic dehydration in a neonate: brain MRI findings

Severe hypernatremic dehydration can cause serious neurological complications in neonates. The most significant problems include brain oedema, intracranial haemorrhage, sinus thrombosis, haemorrhagic infarcts and permanent brain damage. The symptoms of many of these complications are similar. With respect to brain MRI findings in hypernatremic neonates, this is a report that describes linear lesions that represent intracranial haemorrhage at the grey-white matter junction. These MRI findings may be helpful for diagnosing hypernatremic dehydration, and for ruling out differential diagnoses for complications of this disorder.

CRANIAL MR VENOGRAPHY FINDINGS OF SEVERE HYPERNATREMIC DEHYDRATION IN ASSOCIATION WITH CEREBRAL VENOUS THROMBOSIS IN THE NEONATAL PERIOD

Severe neonatal hypernatremia is an important electrolyte disorder that has serious effects on the central nervous system, including brain edema, intracranial hemorrhage, hemorrhagic infarct, and thrombosis. Cerebral venous thrombosis is relatively rare in severe neonatal hypernatremic dehydration. The English literature contains only a few reports of the cranial radiological findings in severe neonatal hypernatremia. The authors report cranial MR venography findings of a newborn infant with severe hypernatremic dehydration. To the best of their knowledge, this is the first such report in the English literature.