Clinical Evidence Of Dehydration Research Articles

Variables Associated With Intravenous Rehydration and Hospitalization in Children With Acute Gastroenteritis

Despite guidelines endorsing oral rehydration therapy, intravenous fluids are commonly administered to children with acute gastroenteritis in high-income countries. To identify factors associated with intravenous fluid administration and hospitalization in children with acute gastroenteritis. This study is a planned secondary analysis of the Pediatric Emergency Research Canada (PERC) and Pediatric Emergency Care Applied Research Network (PECARN) probiotic trials. Participants include children aged 3 to 48 months with 3 or more watery stools in 24 hours between November 5, 2013, and April 7, 2017, for the PERC study and July 8, 2014, and June 23, 2017, for the PECARN Study. Children were from 16 pediatric emergency departments throughout Canada (6) and the US (10). Data were analyzed from November 2, 2018, to March 16, 2021. Sex, age, preceding health care visit, distance between home and hospital, country (US vs Canada), frequency and duration of vomiting and diarrhea, presence of fever, Clinical Dehydration Scale score, oral ondansetron followed by oral rehydration therapy, and infectious agent. Intravenous fluid administration and hospitalization. This secondary analysis of 2 randomized clinical trials included 1846 children (mean [SD] age, 19.1 [11.4] months; 1007 boys [54.6%]), of whom 534 of 1846 (28.9%) received oral ondansetron, 240 of 1846 (13.0%) received intravenous rehydration, and 67 of 1846 (3.6%) were hospitalized. The following were independently associated with intravenous rehydration: higher Clinical Dehydration Scale score (mild to moderate vs none, odds ratio [OR], 8.73; 95% CI, 5.81-13.13; and severe vs none, OR, 34.15; 95% CI, 13.45-86.73); country (US vs Canada, OR, 6.76; 95% CI, 3.15-14.49); prior health care visit with intravenous fluids (OR, 4.55; 95% CI, 1.32-15.72); and frequency of vomiting (per 5 episodes, OR, 1.66; 95% CI, 1.39-1.99). The following were independently associated with hospitalization: higher Clinical Dehydration Scale score (mild to moderate vs none, OR, 11.10; 95% CI, 5.05-24.38; and severe vs none, OR, 23.55; 95% CI, 7.09-78.25) and country (US vs Canada, OR, 3.37; 95% CI, 1.36-8.40). Oral ondansetron was associated with reduced odds of intravenous rehydration (OR, 0.21; 95% CI, 0.13-0.32) and hospitalization (OR, 0.44; 95% CI, 0.21-0.89). Intravenous rehydration and hospitalization were associated with clinical evidence of dehydration and lack of an oral ondansetron-supported oral rehydration period. Strategies focusing on oral ondansetron administration followed by oral rehydration therapy in children with dehydration may reduce the reliance on intravenous rehydration and hospitalization. ClinicalTrials.gov Identifiers: NCT01853124 (PERC) and NCT01773967 (PECARN).

OR25-04 Over 14% of Inpatients with Euvolemic Hyponatremia Have Undiagnosed Adrenal Insufficiency

Background- The commonest cause of euvolemic hyponatremia (EvHNa) is the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The diagnosis of SIADH requires the exclusion of secondary adrenal insufficiency (AI) and untreated hypothyroidism. Studies have suggested about 4% of unselected patients presenting to the emergency room with EvHNa have undiagnosed SAI.1 Among patients admitted to specialized endocrine units this prevalence maybe as high as 20%.2Objective- To study the prevalence of undiagnosed AI among inpatients with EvHNa admitted to general medical wards. Methods- This was a prospective, single centre observational study conducted among inpatients with EvHNa. EvHNa was defined as patients with a serum sodium (Na) <135 mEq/L, with no clinical evidence of dehydration or fluid excess, and a urine spot Na >30mmol/L. In addition patients with recent vomiting, renal failure, recent diuretic use, uncontrolled hyperglycemia and patients with history of use of oral or parenteral steroids in the last 6 months were excluded. Adrenal functions were assessed by a modified porcine ACTH stimulation test which has been described recently by Nair et al. A cut off cortisol value of <18mg/dl after 60 minutes of ACTH injection was used to diagnose AI.3Results- One hundred and forty one (141) patients were included after informed consent and all underwent a modified ACTH stimulation test. They had a mean age of 58 years and 52.3% (n=74) were males. Modified ACTH stimulation testing suggested 20/141 (14.2%) had undiagnosed AI. The mean age among those with AI was 55.2 years. In only 25% (5/20) AI was suspected based on clinical presentation by the treating physician. Despite excluding patients with documented steroid use, the commonest cause of AI (9/20) was secondary AI due to exogenous steroid use including high potency inhaled steroids (5/9) and the use of undocumented steroids or steroid containing medicaments by alternative practitioners (4/9). Hypopituitarism was diagnosed as the cause of AI in 5 patients, which included unsuspected Sheehan’s syndrome in post menopausal women (3/5), non functioning pituitary adenoma (1/5) and lymphocytic hypophysitis (1/5). Despite primary AI not commonly presenting as EvHNa, 3/20 patients had primary AI and in the remaining 3 patients the aetiology of AI remained unclear. Conclusions- Undiagnosed AI is much more common in our country among inpatients presenting with EvHNa to medical units. This increase is primarily driven by inhaled and undocumented exogenous steroid use and undiagnosed Sheehan’s syndrome. An assessment of the hypothalamic-pituitary-adrenal axis is mandatory before making a diagnosis of SIADH. References -(1) Diederich et al. Eur J Endocrinol 2003; 148: 609-617. (2) Cuesta et al. Clin Endocrinol (Oxf) 2016; 85: 836-844. (3) Nair A et al. Eur J Endocrinol. 2019 Oct 1. pii: EJE-19-0558.R2.

Emergent management of primary headache: a review of current literature.

The current article reviews recent data on treatment of acute headache patients in the acute care setting. Intravenous fluid hydration, a common component of emergency department (ED) migraine therapy, does not improve pain outcomes and leads to longer ED lengths of stay. Therefore, intravenous fluids should be administered only to migraine patients with clinical evidence of dehydration. Similarly, intravenous ketamine has garnered interest as a treatment for acute pain but does not provide substantial relief to migraine patients. New studies on the serotonin (5-HT3; 5-hydroxytryptamine-3) antagonist granisetron, intranasal lidocaine, and high-flow oxygen have reported conflicting results for migraine patients. Finally, although experts recommend avoiding opioids in migraine treatment, opioid administration remains prevalent in the ED. A new study has demonstrated that patients who receive intravenous hydromorphone in the ED are much less likely to attain acute headache relief. Standardized headache protocols may decrease opioid use and provide significant pain relief for patients. Recent data have clarified the role of opioids and ketamine in the ED (do not use!). The role of treatment protocols and intravenous fluids is still ill-defined. Subpopulations of migraine patients may benefit from high-flow oxygen and intranasal lidocaine.

Using 24-Hour Weight as Reference for Weight Loss Calculation Reduces Supplementation and Promotes Exclusive Breastfeeding in Infants Born by Cesarean Section.

To promote exclusive breastfeeding, supplements are not recommended without medical indications such as clinical evidence of dehydration. Loss of ≥10% of birth weight (BW) often triggers supplementation due to nursery staff's concern for dehydration. Studies have demonstrated that transplacental passage of maternal intrapartum intravenous fluids for anesthesia may inflate BW. Researchers have proposed using newborn's 24-hour weight (24HW), after fluid diuresis, as preferred reference for weight loss calculation. The mother-infant unit at Hartford Hospital, a Baby-Friendly Hospital, implemented this recommendation into routine practice in March 2014. This study was conducted to evaluate this practice change's safety and effectiveness in decreasing supplementation. We performed a retrospective chart review on healthy full-term newborns delivered by C-section in 12 months before (n = 404) and a 12-month period after (n = 263) incorporating the 24HW into routine practice. Overall supplementation rate, maximum weight loss, length of stay (LoS), and peak transcutaneous bilirubin (TcB) were compared. Overall supplementation rate decreased from 43.6% pre- to 27.4% postintervention and in first-time mothers from 51.9% to 31.0%. Among infants losing ≥10% of BW, the supplementation rate decreased from 63.9% to 26.2%. There was no significant increase in maximum weight loss, peak TcB level, or LoS overall or in those with ≥10% weight loss from birth. Routine use of 24HW as the reference for newborn weight loss calculation reduced supplementation and did not increase untoward effects during the hospital stay.

Pulmonary Embolism Associated with Hyperemesis Gravidarum Two Case Reports

Pulmonary embolism is a major cause of death during pregnancy or the puerperium. The hemostatic changes in pregnancy creates a prothrombotic milieu. Hyperemesis gravidarum is one of the recognised risk factors for venous tromboembolism.Two cases of maternal mortality were attributed to PE associated with severe hyperemesis gravidarum in 2014 in Turkey. These two cases have been reported and discussed in the literature review. We aimed to alert clinicians that thromboprophylaxis should be considered when a pregnant woman suffers vomiting leading to clinical evidence of dehydration.

Index of Suspicion in The Nursery

A 4-day-old male infant presents in late November to the pediatrics clinic with decreased activity and poor feeding. The mother reports that he had been feeding and acting well until 1 day before presentation. The mother states that he has not had any rhinorrhea, nasal congestion, cough, vomiting, diarrhea, rash, or any atypical movements that could be seizures. She had not taken his temperature, and she states that he has not felt hot. The pediatrician becomes immediately concerned as she recognizes a lethargic infant in respiratory distress. A code is called, and the resuscitation is begun. The infant was a 3,083-g product of a 38+1 week gestation to a 28-year-old G2P1 woman. The pregnancy was only complicated by a positive group B streptococcus screen at 35 weeks' gestation and a history of herpes simplex virus in the past, but no lesions were noted before or during delivery. On presentation to labor and delivery, the fetus was noted to be tachycardic and the mother had mild abdominal tenderness, leading to initiation of ampicillin and gentamicin 16 hours before delivery. The duration of rupture of membranes was 4 hours. The infant was born via spontaneous vaginal delivery and was vigorous, with Apgar scores of 9 and 9 at 1 and 5 minutes. Because the mother was neither febrile nor tachycardic, it was decided that she did not have chorioamnionitis, so the infant received no further laboratory evaluation or antibiotics. The mother and infant were discharged from the hospital after 2 uneventful days. In the clinic, the 4-day-old infant has initial vital signs that included a temperature of 98.9°F, a heart rate of 170 beats per minute, a respiratory rate of 71 breaths per minute, an oxygen saturation (SaO2) of 80% on room air, and blood pressure 84/35 mm …

Fulminant pneumococcal meningitis manifesting as acute abdomen

In January 2007, a 21-year-old woman presented to the emergency department with abdominal pain, fever, nausea, vomiting and diarrhoea for 6 hours. She had no other associated symptoms with unrevealing previous history. On examination she was ill-looking, conscious and oriented, with a temperature of 39.2°C, blood pressure 96/52 mmHg and pulse rate 140 beats per minute, and had clinical evidence of dehydration. Her abdomen was rigid, mainly in the right lower quadrant, with sluggish bowel sounds. The rest of the clinical examination was normal including the neurological examination. The results of blood tests were white blood cell count= 19 × 109/litre (normal range (NR) 4–11× 109/litre) with 91% neutrophils, sodium 138 mmol/litre (NR 135–145 mmol/litre), potassium 3.4 mmol/litre (NR 3.5–5 mmol/litre), serum glucose 7.1 mmol/litre (NR 4–6 mmol/litre). A chest radiograph was normal; the abdominal X-ray showed dilated bowel loops and no free gas under the diaphragm. The initial differential diagnosis was gastroenteritis vs acute appendicitis. The normal abdominal ultrasound and normal computed tomography (CT) scan made the diagnosis of appendicitis very unlikely. The patient was admitted as a case of gastroenteritis and improved on intravenous hydration, pain control, and intravenous ciprofloxacin 400 mg 12-hourly and metronidazole 500 mg 8-hourly. Twenty-nine hours after admission she complained of headache, became increasingly lethargic and febrile (39°C), and the abdomen was still rigid. Her level of consciousness deteriorated with Glasgow Coma Scale of 8/15 (eye opening 2/4, verbal response 2/5 and motor response 4/6) and nuchal rigidity was obvious at this stage. Formal neurological exam was not feasible because of the patient's condition, but she was moving all her limbs and had no obvious clinical evidence of lateralizing signs. Bacterial meningitis was suspected and treated with intravenous dexamethasone 6-hourly, ceftriaxone 2 g 12-hourly and vancomycin 1 g 12-hourly. An hour later, while awaiting a CT scan she developed tonic clonic seizures with fixed dilated pupils and was transferred to the intensive care unit where she was immediately intubated and ventilated. CT of the brain was normal (Figure 1). Lumbar puncture revealed a total cell count of 80 × 109/litre with 52% polymorphs and 48% mononuclear cells, protein concentration 8.3 g/litre (NR 0.1–0.4 g/litre), glucose concentration was &lt;0.03 mmol/litre (NR &lt;20 mg/dl), and Gram staining of CSF showed Gram-positive diplococci. Subsequently, CSF and blood cultures yielded Streptococcus pneumoniae sensitive to penicillin so she was given intravenous penicillin G 4 million units 4-hourly. Over 2 days she developed septic shock requiring inotropes, and remained in a deep coma. Magnetic resonance imaging of the brain showed diffuse leptomeningeal enhancement and multiple infarctions in both cerebral hemispheres, the brainstem and cerebellum (Figure 2). Unfortunately the patient never regained consciousness and 5 days after presentation she died despite all supportive measures.

Letters

Objectives Bedside ultrasonography (US) measurement of the inferior vena cava (IVC) and aorta (Ao) may be useful in objectively assessing children with dehydration. The objectives of this study were 1) to compare the IVC and Ao diameters (IVC/Ao) ratio of dehydrated children with controls and 2) to compare the IVC/Ao ratio before and after intravenous (i.v.) rehydration in children with dehydration. Methods This prospective observational study was performed in an urban pediatric emergency department. Children between 6 months and 16 years of age with clinical evidence of dehydration were enrolled. Bedside US measurements of the IVC and Ao were taken before and immediately after i.v. fluids were administered. An age-, gender-, and weight-matched control without dehydration was enrolled for each subject. The IVC/Ao ratios of subjects and controls were compared using Wilcoxon signed rank test, as were the ratios before and after i.v. hydration for each subject. Results Thirty-six pairs of subjects and matched controls were enrolled. The IVC/Ao ratios in the subjects were lower as compared with controls (mean of 0.75 vs. 1.01), with a mean difference of 0.26 (95% confidence interval = 0.18 to 0.35). In subjects, the IVC/Ao ratios were significantly lower before i.v. hydration (mean of 0.75 vs. 1.09), with a mean difference of 0.34 (95% confidence interval = 0.29 to 0.39). Conclusions As measured by bedside US measurement, the IVC/Ao ratio is lower in children clinically assessed to be dehydrated. Furthermore, it increases with administration of i.v. fluid boluses.

Hyperglycemic Hyperosmolar Nonketotic Syndrome in a Child With Acute Lymphoblastic Leukemia Undergoing Induction Chemotherapy

Hyperglycemic hyperosmolar nonketotic syndrome, a life-threatening complication commonly associated with uncontrolled type 2 diabetes mellitus in adults, is characterized by severe hyperglycemia, a marked increase in serum osmolality, and clinical evidence of dehydration without the accumulation of beta-hydroxybutyric or acetoacetic ketoacids. There is a variable alteration in sensorium. The syndrome has been rarely reported in children with leukemia undergoing induction therapy. The authors' aim is to sensitize physicians to this life-threatening illness, which can be treated effectively if diagnosed early.

Acute febrile diarrhoea in horses: 86 cases (1986-1991).

Eighty-six horses presented for examination at the Rural Veterinary Centre between January 1986 to December 1991 with acute diarrhoea. The average age of affected horses was 3.2 +/- 0.2 years (mean +/- SE), with 69% three years or younger. Sixty-one horses were male (36 stallions, 25 geldings) and 83 horses were Thoroughbreds (47) or Standardbreds (36). Sixty-six horses were undergoing routine training at the time of onset of diarrhoea. Eight horses were afflicted with a non-specific illness within one to five days before the onset of diarrhoea, whereas eight horses developed diarrhoea during or within 48 h of discontinuation of antimicrobial therapy. Three horses developed the diarrhoea within 24 h of road transportation. Clinically, the disorder was characterised by a fever, sudden onset of profuse diarrhoea, clinical evidence of dehydration (estimated to be 5 to 12% of body weight at the time of admission) and shock. Degenerative leucopaenia, hyponatraemia, hypochloraemia, hyperkalaemia, hyperglycaemia and azotaemia were characteristic laboratory findings. Laminitis was a sequel in about 30% of cases. The cause of diarrhoea remained undetermined in most cases. Salmonellas were isolated from faecal or tissue samples in only two cases. Similarly, there was no evidence of seroconversion to Erhlichia risticii in 17 cases. Sixty-two of the horses survived the acute phase of the disease in response to supportive care. In horses that did not survive, necropsies were performed and revealed sanguineous or turbid peritoneal fluid. The colonic and caecal walls were oedematous and thickened with serosal congestion and discolouration of these organs evident grossly.(ABSTRACT TRUNCATED AT 250 WORDS)

Treatment of hyperglycaemic hyperosmolar non-ketotic syndrome.

Hyperglycaemic hyperosmolar non-ketotic syndrome (HHNS) is a life-threatening complication of uncontrolled diabetes mellitus. This syndrome is characterised by severe hyperglycaemia, a marked increase in serum osmolality, and clinical evidence of dehydration without significant accumulation of ketoacids. HHNS is typically observed in elderly patients with non-insulin-dependent diabetes mellitus, although it may rarely be a complication in younger patients with insulin-dependent diabetes, or those without diabetes following severe burns, parenteral hyperalimentation, peritoneal dialysis, or haemodialysis. Patients receiving certain drugs including diuretics, corticosteroids, beta-blockers, phenytoin, and diazoxide are at increased risk of developing this syndrome. Patients usually present with a prolonged phase of osmotic diuresis leading to severe depletion of both the intracellular and extracellular fluid volumes. Losses of water exceed those of sodium, resulting in hypertonic dehydration. Therefore, correction of the syndrome will ultimately require administration of hypotonic fluids. Patients presenting with HHNS also have significant depletion of potassium and other electrolytes that will need to be replaced. The principal goal at the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. Precipitating causes of HHNS must be identified and treated simultaneously with correction of the metabolic abnormalities. Appropriate management of precipitating illnesses will limit the high mortality associated with HHNS. This review discusses the current state of knowledge concerning the pathogenesis of HHNS, the clinical features of the disorder, and a systematic approach to treatment.

1816 ANTIDIURETIC HORMONE (ADH) SECRETION DURING RESPIRATORY DISTRESS IN CHILDREN WITH BRONCHOPULMONARY DYSPLASIA (BPD)

Twelve children (age:3 mos to 7 mos, sex:m:f::8:4) known to have bronchopulmonary dysplasia were studied for antidiuretic hormone response during hospitalization with respiratory distress, hypoxemia and hyperinflation on chest x-ray. 7/12 had wheezing at the time of admission. None had received any medications before admission. None of the children had clinical evidence of dehydration (normal plasma renin activity of 2.4–4.7 ng/ml). Plasma ADH levels were measured by radioimmune assay (N=up to 1.7 mU/ml) and were elevated 6–9 fold (2.4 mU/ml–3.1 mU/ml) within 7–10 days. 3/12 children developed hyponatremia (129–131) 24 hours after admission. Further, 2/3 children with hyponatremia developed diastolic hypertension for up to 2 days. 7/12 were given furosemide at the time of admission for the presence of wheezing. Though the wheezing diminished considerably following furosemide, there was no reduction in the plasma ADH levels. We conclude that 1. ADH secretion is common in children with BPD during acute respiratory distress 2. The mechanism for the production of ADH is either hypoxemia and/or hyperinflation 3. Hyponatremia occurs with increased ADH secretion and therefore care should be exercised in the administration of fluids 4. Though furosemide may have a beneficial effect on the respiratory distress in children with BPD, the plasma ADH levels are not influenced by its administration and 5. The continued ADH secretion in children with BPD feeds a vicious cylcle.

Letters to the Editor

The commentary was not a report on a controlled study but an outline of our management of severe infantile gastroenteritis. We define this as acute diarrheal disease in children less than 1 year of age of such severity that there is clinical evidence of dehydration and intravenous fluids are required to restore hydration to normal. These infants require admission to a hospital and are at least 5% dehydrated. We classify the diarrhea as persistent if it is still present seven days after admission and the infant still requires intravenous fluids to maintain hydration.

Inadequacy of Fractional Excretion of Sodium Test-Reply

We were interested to see the low fractional excretion of sodium and the high urine-to-plasma ratio of creatinine in the patient with acute renal failure after contrast studies described by D'Elia et al. We concur that these urinary indices can be deceiving and can lead to inappropriate and hazardous fluid volume challenges in patients with oliguria. In the patients we described, there was no clinical evidence of dehydration on examination and, in two patients who required hemodynamic monitoring for their underlying disease processes, volume status and cardiac status were clearly adequate. Further volume expansion in these patients clearly would lead to further complications.