The Risk Of Cerebral Oedema In Children Essay
The Risk Of Cerebral Oedema In Children Essay
Over-hydration in diabetic ketoacidosis (DKA)
may increase the risk of cerebral edema in
children.
Patients
Fourty five pediatric patients (1 month–16 years) presenting with 41 episodes of DKA.
Intervention The clinical and biochemical variations was selected by the hospital during the date of their hospital admission. Dehydration was calculated by measuring acute changes in body weight during the period of illness. The Risk Of Cerebral Oedema In Children Essay.
Results
The magnitude presentation of the centile 25~35 percent was in the ratio of 5.6% (3.4–8.2%) (mean±SD 6.1±4so there was no clinical and biochemical assessment variation was needed. These both of the variations ,all of the diabetic ketoacidosis patient approached. Further all the patient variation w not correlated with the amplitude of variation and magnitude presentation and did not affect the fluid concentration and the quantity of the fluid was 47.8 ml/kg (36.5–56.3)) in the first 12 hours.
Conclusion
For the conclusion of the exact perimeters and the magnitude variations of the fluid in the patients of diabetic ketoacidosis. All of the conformations needs study on the larger scale.
MATERIALS AND METHODS
We conducted a prospective study of consecutive patients aged 1 month–16 years, diagnosed with DKA, who presented to the emergency department in a xinjiang medical university hospital
from January 2010 to February 2012.The study was approved by the Ethics Committee of the First Affiliated Hospital of Xinjiang Medical University, this study was done in the declaration of Helsinki.
. Patients were excluded from the study when patient and/or parental consent was not obtained, or when fluid replacement therapy had begun prior to weighing the patient. DKA was defined as a pH <7.3 (venous), a glucose >11 mmol/l, calculated
bicarbonate (HCO3) of <15 mmol/l and the presence of urine ketones.1 Recovery from DKA was defi ned as HCO3 ≥18 mmol/l. Blood gases were assessed at least every 2 h in the first
12 h and at least every 4 h in the next 24 h. The Risk Of Cerebral Oedema In Children Essay. The following clinical variables were collected on admission: demographics, heart rate, arterial blood pressure, capillary refill time and level of consciousness using the Glasgow Coma Scale (GCS). The laboratory results recorded on admission included: blood gases, glucose, hemoglobin, haematocrit, electrolytes, osmolality, creatinine, blood urea nitrogen (BUN), HbA1c, albumin and lactate levels. The osmolar gap (measured osmolality−calculated osmolality) was calculated. 12 Sodium (Na+) was corrected for glucose level ([Na+]+([ glucose]−5.6)/5.6)×1.6). Deviation of the heart rate and blood pressure from the mean and maximum normal values for age were calculated for each patient.12 Weight was obtained on admission before fluid administration (admission weight).
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and every 12 h thereafter until discharge from hospital (discharge weight) and until two consecutive similar weights (0.5%) were obtained (final weight). In the absence of two
consecutive similar weights, the patient’s weight within 7 days after discharge was considered as the final weight. The magnitude of dehydration was defined as the % loss of
body weight (LBW) ((discharge weight−admission weight)/ discharge weight×100).. An average of three readings were recorded. The calculated coefficient of variation (SD/
mean×100) of the scales was a mean of 0.21% for patients over 15 kg and 0.34% for those under 12 kg. After the study, we retrospectively examined the charts for the actual amount of fluid administered to each patient. The Risk Of Cerebral Oedema In Children Essay.For determining the percentage of fluid above maintenance, the
maintenance amount of fluid was calculated according to the following: 100 ml/kg for the first 10 kg, 50 ml/kg for the next 10–20 kg and 20 ml/kg thereafter12 All patients were managed according to a pre-existing provincial management protocol (endorsed by the Province of china xinjiang) for fluid, insulin and electrolyte administration In brief, on admission, each patient initially received 10 ml/kg measured weight of 0.9% saline, repeated as necessary until haemodynamic stability was achieved as judged by the responsible physician. This was followed by an infusion o f 0.9% or 0.45% saline at a rate of 4–6 ml/kg/h (independent of age and urine output) until DKA resolved. Potassium and glucose were added to the solution as necessary.
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Table 1 Demographic characteristics of all analyzed patients on admission with diabetic ketoacidosis episodes
Age (years)
11 (5–16)
New diabetes (%)
52.6
Male (%)
47.8
Weight (kg)
35.4 (18.3–56.9)
Fluid (ml/kg/12 h)*
52.9 (45.0–66.7)
Fluid over calculated maintenance (%)
107 (51–148)
Calculated degree of dehydration (%)
5.7 (3.7–8.1)
Length of stay (h)
30 (24–48)
Duration of symptoms (days)
5.0 (2–16)
PCCU admission (%)
21.1
pH
7.12 (7.05–7.22)
Na+ (mmol/l)
133 (130–135)
Na+ corrected (mmol/l)
140.4 (136.9–143.9)
Glucose (mmol/l)
33.3 (25.2–43.6)
Chloride (mmol/l)
96.5 (94–103)
Haematocrit 0.44 (0.41–0.48)
0.44 (0.40–0.48)
Hemoglobin (mg/dl)
13.3 (12.3–14.7)
*First 12 h including resuscitation fluid. PCCU, pediatric
Statistical analysis
SPSS V.16.0 was used for data analysis. Categorical data were summarized as percentages. The results were reported as medians (25th–75th centiles).
The Pearson correlation coefficient was used to assess the relationship between normally distributed continuous variables, and Spearman.s rho was used for skewed continuous
variables. The Risk Of Cerebral Oedema In Children Essay.The χ2 test or Fisher’s exact test was used to compare differences in proportions for categorical variables. The independent samples t test was used to compare mean differences
in normally distributed continuous outcomes, and the Mann–Whitney U test was used to compare skewed continuous variables between categorical independent variables. A p value of <0.05 was considered statistically significant except when the Bonferroni adjustment was made for multiple comparisons.
RESULTS
During the study period, 49 patients with 53 episodes of DKA were managed in our centre. Six patients had commenced treatment prior to arrival and were not eligible for the study. Four
of the 43 eligible patients declined to participate. Therefore, 39 patients with 42 episodes of DKA were successfully enrolled and completed the study.
Demographics
Demographic data are provided in table 1. All patients had type 1 diabetes. Nine of the patients (21%) were admitted to the pediatric intensive care unit. The rest were admitted to
the pediatric medicine department. Only three patients (7.35 %) presented with a GCS <13. One patient (2.69%) presented with mild hypothermia (32.9°C) and required mechanical ventilation. The Risk Of Cerebral Oedema In Children Essay.
No patient experienced a decreased GCS after initiation of therapy and all had attained a GCS >13 within 12 h of commencing treatment
TABLE 2
Association between demographic, clinical and biochemical variables recorded on admission and magnitude of dehydration
Categorical variables p* Value
PCCU admission
0.783
New diabetes
0.623
Lactate >2.2 mmol/l
0.748
Continuous variables
r Value
p‡ Value
Age (years)
−0.192
0.216
pH 0.146 0.363
0.1444
0.360
HCO3 0.057 0.720
0.055
0.718
Glucose
0.203
0.200
Sodium [Na+]
0.355
0.018
Corrected sodium [Na+]
0.501
0.001
Potassium (K+)
0.210
0.172
Creatinine
0.207
0.179
Blood urea nitrogen
0.276
0.071
CO2
0.040
0.790
Creatinine
0.209
0.179
Creatinine†
0.281
0.065
Anion gap
0.047
0.632
Anion gap (corrected)
0.050
0.752
HbA1c
−0.028
0.870
Osmolality
0.223
0.151
Osmolality (gradient)
0.003
0.984
Fluid (ml/kg/12 h)
0.111
0.477
Fluid (% above maintenance)
0.011
0.935
Mean heart rate†
0.041
0.777
Respiratory rate
− 0.118
0.448
Mean blood pressure†
− 0.101
0.427
Length of stay
0.097
0.557
Duration of symptoms
−0.154
0.307
*Calculated using the t test and Mann–Whitney U test.
†Levels above normal values corrected for age.
‡Calculated using the Pearson correlation coefficient for normally distributed
continuous variables; Spearman’s rho was used for skewed continuous variables. The Risk Of Cerebral Oedema In Children Essay.
PCCU, pediatric critical care unit
Correlation of dehydration with biochemical or clinical
parameters on admission
In the study population, the median (25th–75th centiles) magnitude of dehydration, based on LBW, was 5.7% (3.7–8.3%) (range 1.4–24.8%) or 8.9% (6.0–13.5%) (range 1.9–41.0%) when corrected for % of total body water. In 20/42 (48%) episodes, parents had noted weight loss in their child. No
significant correlations were found between the patient’s demographic variables (age, duration of symptoms, new versus known diabetes), clinical variables (deviation of heart rate
from maximal rate corrected for age or deviation of mean arterial blood pressure corrected for age) or biochemical variables (pH, HCO3, glucose, CO2, HbA1c, creatinine and BUN deviation
from maximum normal values, anion gap, corrected anion gap, osmolar gap and the presence of lactic acidosis) recorded on admission and the magnitude of dehydration, whether
based on LBW or corrected for % of total body water (table 2). Sodium and corrected sodium level were the only biochemical variables to show reasonable correlation with severity of
dehydration (r=0.35, p=0.02 and r=0.502, p=0.001, respectively). The Risk Of Cerebral Oedema In Children Essay.Although no significant correlation between patient age and the magnitude of dehydration was observed across the whole group, when we subdivided the patients, based on age, into those ≤2 years and >2 years of age, the magnitude of dehydration in children ≤2 years of age (n=6) was significantly greater whether expressed in LBW (9.7% (6.2–11.8%) vs 5.3% (3.5–7.4%), p=0.014) or corrected for total body water (15.2% (10.5–18.5%) vs 8.3% (5.5–10.7%), p=0.016). The Risk Of Cerebral Oedema In Children Essay.
Categorizing the magnitude of dehydration to non-severe
and severe
Severe dehydration (LBW ≥6% in children, ≥10% in infants)12 was detected in 18/42 (43%) patients. The main characteristics of patients with non-severe (mild, moderate) and severe
dehydration are presented in table 3. Except for the corrected [Na+] on admission, no significant differences were observed between groups.
Correlation between magnitude of dehydration and amount
of fluid administered
In the first 12 h, fluids were administered exclusively via the intravenous route. The median (25th-75th centiles) volume of administered during the first 12 h was 52.9 ml/kg (45-66.4 ml/kg). No correlation was detected between the total amount of fluid administered or the amount of fluid administered
above maintenance and the magnitude of dehydration (figure 1). There was, however, a negative correlation between the amount of fluid administered during therapy and the pH on admission (r=−0.44, p<0.05).
Resolution of DKA
In all patients, DKA resolved within 24 h (figure 2). No significant elations were found between the patient’s age, ew versus known diabetes, glucose level, osmolar gap, presence
of lactic acidosis, magnitude of dehydration on admission r amount of fluid administered in the first 12 h (whether expressed as ml/kg or % above maintenance) and the rapidity
of recovery from DKA (figure 2). However, there was a significant negative correlation between the level of HCO3 on admission and time to recovery (r=−0.74, p<0.001).
DISCUSSION
Fluid replacement is the cornerstone of therapy in DKA. Work n animal models demonstrates that successful fluid replenishment lone will reverse many of the clinical and biochemical
derangements seen in DKA. However, precise fluid therapy is often impeded by difficulties in the determination f the magnitude of dehydration in DKA and differences in
opinion regarding the need to account for on-going fluid (urinary) loss. The mean magnitude of dehydration observed in his study is similar to that reported in previous studies4 and
supports current recommendations to assume a 7–10% depletion n total body water when managing patients in DKA.1 14 these recommendations are based mainly on two studies
performed in 195215 and 193316 in a small number of patients. he observation that children ≤2 years of age had a significantly higher degree Of dehydration has also been reported
previously.17 It is speculated that younger children, who can either independently gain access to fl uids nor successfully ommunicate symptoms, experience a greater degree of
dehydration and acidosis.18 19 despite reports that severe dehydration is rare in
DKA,1 4 5 severe dehydration was observed in 18/42 (43%)Patients in this study, a higher proportion than recorded in he studies of Harris et al 7 (23.7%) and Fagan et al 4 (12%). The Risk Of Cerebral Oedema In Children Essay.
This difference could be due to different patient demographics, Such as the large geographical size of our referral region and subsequent delays in transport for definative treatment.16
Table 3
Comparison of vital signs, serum markers and demographics between those with mild, moderate
and severe dehydration*
Non-severe dehydration (n=24) Severe dehydration (n=18) p Value
Age (years)
11.5 (7–15)
11.0 (5–14.2)
0.703
Duration of symptoms (days
6 (3–28)
5.0 (1–14)
0.40
Length of stay (h)
30 (24–48)
30 (24–49
0.858
PCCU admission (%
5 (19.8)
4 (21.2)
0.74
New diabetes (%)
13 (54.6)
8 (49.0)
0.98
Delta heart rate mean (bpm
42.7 (12.4–52.8)
41.9 (30.0–51.6)
0.70
HbA1c (%)
11.9 (10.8–12.9)
11.2 (10.0–13.6)
0.35
pH
7.11 (7.03–7.22)
7.20 (7.05–7.21)
0.35
HCO3 (mmol/l)
8 (6–12.5)
10.5 (6–11)
0.46
Anion gap corrected
27.1 (25.4–33.2)
28.6 (25.3–29.9)
0.80
Glucose (mmol/l)
32.1 (25.8–42.9)
35.7 (27.9–43.9)
0.32
Blood urea nitrogen (mmol/l)
6.9 (4.6–9.6)
7.5 (6.5–12.2)
0.19
Cr (μmol/l)
90 (61.5–133.5)
105 (75–136)
0.559
Lactate (mmol/l)
2.2 (1.4–2.6)
2.3 (1.5–3.3)
0.51
Na+ (mmol/l)
133 (128–135)
134 (132–136)
0.273
Na+ corrected (mmol/l)
138.2 (136.5–143.0)
141.3 (140.7–144.5)
0.036
Osmolality (mOsm/kg)
329 (317–337)
329 (320–350
0.413
Osmolar gap (m0sm/kg)
46.4 (41.5–58.7)
47.9 (37.2–62.2)
0.95
Fluid (ml/kg/12 h)
50.2 (34.7–58.1)
51.6 (45.8–59.4
0.89
Fluid over the calculated maintenance (%)
111 (60–145)
91 (66–146)
0.60
Values are median (25th–75th centiles).
*Dehydration was subcategorized based on change in body weight during diabetic ketoacidosis (severe: >6% in children,
>10% in infants).
AG, anion gap; PCCU, paediatric critical care unit.
This study did not demonstrate a significant correlation between comprehensive biochemical, clinical or demographic characteristics of the patients and magnitude of dehydration.
This is consistent with recent studies, which indicate that clinicians failed to predict the magnitude of dehydration accurately when employing more selective clinical or biochemical
patient data.4 5 8 20 It is therefore not surprising that the amount of fluid administered did not correlate with the magnitude of dehydration (figure 1). We speculate that the replacement fluid administered reflects the physician’s subjective impression of the patient’s degree of distress. The Risk Of Cerebral Oedema In Children Essay. However, the patient’s ‘ill’ appearance in DKA may be affected by factors other than fluid deficit, such as acidosis, which can alter level of consciousness, affect perfusion by vasoconstriction and stimulate Kussmaul’s respirations which results in dry mouth.5 It is these factors that may explain the negative correlation between pH and the observed amount of fluid administered in this study. The inability to clinically estimate the level of dehydration in children with DKA with accuracy may in part reflect a relatively well preserved intravascular volume. Furthermore, urine output(usually a sensitive marker of dehydration) is maintained
by a glucose driven diuresis.21All patients were treated in accordance with a provincial
guideline for DKA management, consistent with the ESPE/ LWPES consensus statement. The median volume of fluid administered in the first 12 h of therapy was 3.7 ml/kg/h (3.0–4.6%) (range 2.1–8.3ml/kg/h), which is a more restrictive (about 25% less) regimen than recommended in the literature.22 Despite a wide range of fluid deficit observed in this study, all patients achieved resolution of DKA within 24 h of treatment initiation, independent of severity of dehydration or amount of fluid administered (figure 2). The patients’ weight gain achieved between hospital admission and DKA resolution (median 3.4%, data not presented) was approximately 65% of the patient’s calculated dehydration (median 5.6%). Hence,
Figure 1 Correlation between fluid administered and magnitude of
dehydration, including initial boluses given on admission (r=0.23,
p>0.05). The Risk Of Cerebral Oedema In Children Essay.
this suggests that biochemical resolution in DKA is achieved without full rehydration of the patient. In the absence of a validated method of assessing dehydration in DKA, one should be careful about using the patient’s clinical status to drive fluid replacement therapy. No patient experienced permanent neurological impairment. This suggests that, unless the patient is haemodynamically unstable, it is not necessary to aggressively correct fluid deficit. We believe this is an important and novel finding, as one can then assume that the restrictive strategy of ‘one size fits all’ for rehydration is safe and effective. The validity of this study is subject to a number of limitations. Caution needs to be taken when interpreting several of the study findings because our patient group is relatively small. The Risk Of Cerebral Oedema In Children Essay.
Figure 2 Relationship between time to diabetic ketoacidosis
resolution and degree of dehydration (column), volume of fluid
administered in the first 12 h of therapy (■) and the admission serum
bicarbonate level (Δ). Significant correlation (negative) was found only
between the level of bicarbonate on admission and time to resolution
(r=−0.74, p<0.001).
and the groups are unequal. For example, the findings in table 3 that do not show significant differences may be a reflection of lack of power. Given our small sample size, as well as
the weak correlations and non-significant relationships of the majority of the biochemical and clinical variables with severity of dehydration (table 2), a multivariable regression model
was not performed, which would have allowed us to control for confounding variables (table 2). Although acute weight loss is accepted as the gold standard for quantifying the magnitude
of dehydration,4 6 7 the robustness of the correlation is somewhat understudied. Furthermore, some may argue that the final weight of the patient better reflects total fluid loss rather
than the discharge weight which was used in our study and by others,4 5 especially since DKA and, in particular, new onset DKA, is characterized by an acute catabolic state, which results
in weight reduction from the loss of lean body mass, as well as from concomitant dehydration. The Risk Of Cerebral Oedema In Children Essay.We believe that the final weight reflects the weight gain of lean body mass, which occurs with the introduction of insulin, rather than fluid loss alone.
CONCLUSION
Children in DKA present with a median (25th–75th centiles)dehydration of 5.7% (3.4–8.3%) (mean}SD 6.8}5.0%); however, there is large variability among patients (range 1.4–24.8%).
Since the magnitude of dehydration cannot be assessed accurately by either clinical or biochemical parameters, clinicians should not attempt to administer fluid according to subjective estimates of dehydration. Unless the patient is haemodynamically unstable, a relatively restrictive regimen of fluid administration
BACKGROUND—Cerebral oedema is a major cause of morbidity and mortality in children with insulin dependent diabetes.
AIMS—To determine the risk and outcome of cerebral oedema complicating diabetic ketoacidosis (DKA).
METHODS—All cases of cerebral oedema in England, Scotland, and Wales were reported through the British Paediatric Surveillance Unit between October 1995 and September 1998. All episodes of DKA were reported by 225 paediatricians identified as involved in the care of children with diabetes through a separate reporting system between March 1996 and February 1998. Further information about presentation, management, and outcome was requested about the cases of cerebral oedema. The risk of cerebral oedema was investigated in relation to age, sex, seasonality, and whether diabetes was newly or previously diagnosed.
RESULTS—A total of 34 cases of cerebral oedema and 2940 episodes of DKA were identified. The calculated risk of developing cerebral oedema was 6.8 per 1000 episodes of DKA. This was higher in new (11.9 per 1000 episodes) as opposed to established (3.8 per 1000) diabetes. The Risk Of Cerebral Oedema In Children Essay.There was no sex or age difference. Cerebral oedema was associated with a significant mortality (24%) and morbidity (35% of survivors).
CONCLUSIONS—This first large population based study of cerebral oedema complicating DKA has produced risk estimates which are more reliable and less susceptible to bias than those from previous studies. Our study indicates that cerebral oedema remains an important complication of DKA during childhood and is associated with significant morbidity and mortality. Little is known of the aetiology of cerebral oedema in this condition and we are currently undertaking a case control study to address this issue.
We aimed to evaluate risk factors and outcome of cerebral edema in children with diarrhea.
Methods:
In this retrospective chart analysis, data of all diarrheal children under 5 years of age having convulsion and admitted in intensive care unit were retrieved from an electronic medical record system of Dhaka Hospital of International Centre for Diarrhoeal Disease Research, Bangladesh, from 1st January 2011 to 31st December 2016. Comparison of clinical and laboratory characteristics was made between children with (cases = 22) and without cerebral edema (controls = 66).
Results:
Cases more often had a fatal outcome than controls (36% vs 8%, p = 0.003). In logistic regression analysis, after adjusting for potential confounders, the cases were independently associated with respiratory distress (odds ratio = 5.5, confidence interval = 1.55–19.62, p = 0.008), severe sepsis (odds ratio = 4.6, confidence interval = 1.24–16.77, p = 0.022), and severe malnutrition (odds ratio = 0.16, confidence interval = 0.04–0.74, p = 0.019). A rapid drop (>0.5 mmol/L per hour) in serum sodium did not have any impact on developing cerebral edema (p = 0.090). The Risk Of Cerebral Oedema In Children Essay.
Conclusion:
Identification of simple clinical predictors may help in the early treatment of cerebral edema that may further help in reducing deaths in such children especially in resource-poor settings. However, further research with prospective design is needed to consolidate our observation.
Introduction
Cerebral edema is one of the life-threatening conditions that occur due to the accumulation of a large amount of water in the spaces of the brain.1 Cerebral edema causes loss of subtle cerebral functions,2 so that its early recognition and treatment should not be neglected. Cerebral edema usually presents with alteration in the level of consciousness, the appearance of bradycardia, rise in blood pressure, abnormal breathing patterns, evidence of extraocular movement abnormalities, alteration and inequality of pupillary size, and extensor plantar response on the side of the lesion.1 In acute encephalitis, preceding seizures and status epilepticus are important risk factors for fulminant cerebral edema.3 Hyperammonaemia (⩾200 μmol/L) in case of reduced hepatocyte function and during rapid correction is considered to be a risk factor for cerebral edema.4
There are different causes of cerebral edema. Infective causes include meningitis, encephalitis, toxoplasmosis, and subdural empyema.1 Non-infective causes include trauma or head injury,5 diabetic ketoacidosis,1,6 massive cerebral infarction, ischemic stroke, intracerebral hemorrhages, brain tumor, hypoxia, other toxic or metabolic factors,7 dysnatremia,8 fulminant viral hepatitis, hepatic encephalopathy, systemic poisoning, syndrome of inappropriate antidiuretic hormone secretion (SIADH), opioid drug abuse and dependence, bites of certain reptiles and marine animals, and high-altitude cerebral edema.1 However, there is no such study that looked for the risk factors of developing cerebral edema in children hospitalized for a diarrheal illness in a critical care ward. Intensive care unit (ICU) of the Dhaka hospital of International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b) treats a lot of cases with convulsion.9Some of them had cerebral edema and often ended up with a fatal outcome. Thus, our aim was to find out the risk factors of cerebral edema in diarrheal children and their outcome after treatment. The Risk Of Cerebral Oedema In Children Essay.
Methods
Ethical statement
This is a retrospective chart analysis of the data that were initially obtained for patient management at Dhaka Hospital of icddr, b; patients or caregivers were not asked for an interview. The data were anonymized before they were retrieved. The written approval of the study was taken by the Institutional Review Board (IRB) of icddr, b, comprised of Research Review Committee (RRC) and Ethical Review Committee (ERC) of icddr,b.
Study design
We performed a retrospective chart analysis with an unmatched case-control design. All children of either sex, aged 0–59 months, admitted in the ICU with documented convulsion either at admission or after admission in ICU from 2011 through 2016 constituted the study population. Convulsive children who were assessed to have cerebral edema constituted the cases, and those without cerebral edema constituted the controls. We have only scope to diagnose cerebral edema depending on fundoscopy. On that basis, we did not find the features of cerebral edema in the control group. Controls were taken by randomization, which was 3-fold of the cases. In convulsing children, fundoscopic documentation10 of papilledema (blurring of optic disk margin, other than medial margin which is a normal variant11) was considered as a surrogate marker of cerebral edema. Fundoscopy was done multiple times a day, minimum once.The Risk Of Cerebral Oedema In Children Essay. It is prudent to mention that Dhaka hospital of icddr,b has no brain imaging (MRI, CT-scan) or intracranial pressure monitoring7 facilities, and it is also not possible to send a clinically unstable child for imaging in a distant center. Presence of papilledema was diagnosed by attending physician and thereafter confirmed by a qualified pediatric intensivist (either M.C. or F.A.). Another objective criterion in diagnosing papilledema was the disappearance of blurring of an optic disk partially or completely within 24 h of initiation of treatment with either mannitol or 3% NaCl. After 6–8 h of each dose of mannitol, the response was evaluated by repeating the fundoscopic examination.
Study setting
The study children were admitted and treated at the ICU of the Dhaka Hospital of icddr,b. Description of the study site has been provided elsewhere.12 ICU has the facilities for inotrope support, central oxygen support, noninvasive ventilation and mechanical ventilation in case of respiratory failure, and machine for continuous monitoring support. Data are documented in the electronic server of the hospital by ICU doctors. ICU team comprises of 9 doctors and 14 nurses with other supporting staff. Five junior doctors work according to the roster over 24 h. They are directly supervised by two mid-level physicians and finally overseen by two senior pediatric intensivists.
Patient management
Both the cases and the controls received anticonvulsant. In the ICU, they were followed up by ophthalmoscopy to detect cerebral edema if there was an alteration of mentation or irregular respiration. No children in the control group developed papilledema. The cases additionally received either mannitol or 3% NaCl. No child developed rebound raised ICP post mannitol. Hydration status was also routinely checked in every patient and found to be normal.
We treated hypernatremia by using G-ORS following Adrogue and Madias.13 Patients who were kept nothing per oral for their clinical management perspective, their hypernatremia were treated with ½ strength Normal Saline and 5% dextrose. Fluid resuscitation was given to children with severe sepsis.14 Inotropes were used for children who had septic shock. Bubble CPAP (continuous positive airway pressure), noninvasive ventilatory support was used for children having severe pneumonia with hypoxemia.12 Mechanical ventilators were used in case of respiratory failure. Other management of the patients was done following a standardized protocol followed in the Dhaka hospital of icddr,b and the other management of hospitalized patient has also been described elsewhere.15
Measurements
Case report forms (CRFs) were developed, pretested, and finalized for the acquisition of relevant data. Characteristics analyzed included age, sex, severe malnutrition (severe wasting (z score for weight for height/length <−3 of World Health Organization (WHO) growth standard), or severe underweight (z score for weight for age <−3 of WHO growth standard) or edematous malnutrition), presence of cough, respiratory distress, presence of vomiting, presence of fever (axillary temperature ⩾ 38ºC), presence of severe sepsis (sepsis-induced tissue hypoperfusion or organ dysfunction),16responsiveness, ileus, features of heart failure or fluid overload, presence of pneumonia, respiratory rate, hypoglycemia (<3 mmol/L), rapid drop in serum sodium (>10 mmol/L per 24 h), hyperkalemia (>5.3 mmol/L), hypokalemia (<3.5 mmol/L), hypernatremia (>150 mmol/L), hyponatremia (<135 mmol/L), metabolic acidosis (TCO2 < 18 mmol/L), hypocalcemia (<2.12 mmol/L), hypomagnesemia (<0.65 mmol/L), raised creatinine (1.5 times of upper limit of normal for age), growth of micro-organism in blood culture and rectal swab culture, duration of hospital stay, development of healthcare associated infection (evidence of new infections that was identified at least after 48 h of admission),17,18 and outcome. The Risk Of Cerebral Oedema In Children Essay.
Sample size calculation
During the 6-year study period, we have screened 1225 children under 5 years of age who presented with convulsion to the ICU, and only 22 fulfilled the criteria of cases; from the remaining patients, three controls for each case were selected randomly; thus, there were 66 controls.
Analysis
All data were entered into a personal computer and edited before analysis using SPSS for Windows (Version 20.0; IBM Corp., Armonk, NY) and Epi Info (version 7.0; Epi Info™ software; Centers for Disease Control and Prevention, Atlanta, GA, USA). Differences in proportions were compared by the chi-square test. To compare the means of normally distributed data, Student’s t-test was used and for comparison of data that were not normally distributed, Mann–Whitney test was used. A probability of less than 0.05 was considered statistically significant. The strength of association was determined by calculating the odds ratio (OR) and their 95% confidence intervals (CIs). Variables identified as significant in the bivariate analysis were used as independent variables to develop a predictive model using logistic regression. The dependent variable in that model was cerebral edema. Thus, independent risks for cerebral edema were identified using stepwise logistic regression analysis after controlling for the covariates.
Results
Median (inter-quartile range) age of the study children was 9.5 (4.3–16.5) months among cases and 8 (5.37–14) months among controls. Both the cases and controls had higher male child, 73% and 58% respectively (Table 1). In bivariate analysis, the cases most often found to have respiratory distress and severe sepsis and less likely to be severely malnourished compared to the controls (Table 1). The cases require more days to recover (Table 1), more often required a blood transfusion, mechanical ventilation and had higher case-fatality-rate compared to the controls (Table 2). Laboratory parameters were also similar in both groups. In all, 38 patients had hypernatremia (11 with cerebral edema and 27 without cerebral edema) (Table 3) and were treated by using G-ORS. Rapid drop of serum sodium (>10 mmol/day) was observed in 41% of cases and 20% of controls, and the difference was statistically insignificant. Other variables in Tables 1and and33 were comparable among the groups. In logistic regression analysis, after adjusting for potential confounders, the independently associated factors for cerebral edema in diarrheal children under 5 years of age with convulsion were respiratory distress, severe sepsis, and severe malnutrition (Table 4). The Risk Of Cerebral Oedema In Children Essay.
