Dersleri yüzünden oldukça stresli bir ruh haline sikiş hikayeleri bürünüp özel matematik dersinden önce rahatlayabilmek için amatör pornolar kendisini yatak odasına kapatan genç adam telefonundan porno resimleri açtığı porno filmini keyifle seyir ederek yatağını mobil porno okşar ruh dinlendirici olduğunu iddia ettikleri özel sex resim bir masaj salonunda çalışan genç masör hem sağlık hem de huzur sikiş için gelip masaj yaptıracak olan kadını gördüğünde porn nutku tutulur tüm gün boyu seksi lezbiyenleri sikiş dikizleyerek onları en savunmasız anlarında fotoğraflayan azılı erkek lavaboya geçerek fotoğraflara bakıp koca yarağını keyifle okşamaya başlar
Reach Us +44 3308186230

GET THE APP

Neonatal and Pediatric Medicine - Correlation of Renal Function with Severity of Hypoxic Ischemic Encephalopathy (HIE) in Egyptian Full Term Neonates
ISSN: 2572-4983

Neonatal and Pediatric Medicine
Open Access

Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)

Correlation of Renal Function with Severity of Hypoxic Ischemic Encephalopathy (HIE) in Egyptian Full Term Neonates

Mohamed Abdelaziz El-Gamasy1*, Mohamed M Abdelmageed1, Ahmed R Fakhreldin2, Mostafa M Mehrez1, Mohamed A Nassar1 and Redha Alarabawy3
1Department of Pediatrics, Tanta University, Egypt
2Department of Pediatrics, Aswan University, Egypt
3Department of Diagnostics Radiology, Tanta University, Egypt
*Corresponding Author: Mohamed Abdelaziz El-Gamasy, Department of Medicine, Tanta University, Egypt, Tel: 201208136076, Email: mgamsy@gmail.com

Received: 24-May-2018 / Accepted Date: 22-Jun-2018 / Published Date: 29-Jun-2018 DOI: 10.4172/2572-4983.1000157

Keywords: Renal function; Hypoxic ischemic encephalopathy

Introduction

Hypoxic ischemic encephalopathy (HIE) is one of the most important causes of neonatal morbidity and mortality worldwide. 25% of neonates with HIE develop severe and permanent neurological sequelae including mental retardation, cerebral palsy and epilepsy [1]. Hypoxic ischemic insult triggers a cascade of adverse events that leads to irreversible neuronal and white matter injury over a period of hours to days. Cellular loss occurs in the up new therapeutic modalities for HIE and the increasing knowledge about the pathogenesis of asphyxiarelated disorders, it is often difficult to predict which newborn will develop renal perinatal asphyxia lack specificity, implicating the need for predictors for adverse renal outcomes in infants with HIE [2].

Aim of the Work

To evaluate the level of serum creatinine in newborns with HIE and to assess its correlation with degree of HIE severity according to Sarnat and Sarnat scoring and according to brain CT findings.

Subjects and Methods

This prospective case-control study was conducted on 72 neonates who were classified into two groups:

Group (1) included 36 full term neonates (Their gestational age ranged from 37-42 weeks) who were diagnosed as HIE and admitted to the Neonatal Intensive Care Unit (NICU) of Tanta University hospital (TUH) from April 2017 till April 2018.

Neonates were diagnosed with HIE according to World Health Organization (WHO) definition of HIE if they had demonstrated at least two of the following findings: APGAR score <3 at 1 minute or <6 at 5 minutes, arterial pH <7.2 with base deficit >10 mmol/l, and the presence of post natal clinical complications attributed to birth asphyxia, such as seizures, abnormality in state, hypotension requiring inotropic support, severe apnea and oliguria.

Neonatal AKI was diagnosed according to criteria of Kidney Disease Improving Global Outcome (KDIGO) [3].

Group (2) included 36 age- and sex-matched, apparently healthy neonates who were recruited as a control group.

Exclusion criteria:

-If increased serum creatinine was attributed to causes other than HIE such as hypovolemia, sepsis or localized infection.

-If they were diagnosed with life threatening congenital anomalies, inborn errors of metabolism or preterm births.

This study was done after taking consents from parents of included subjects and approval from Research Ethical Committee of Tanta Faculty of Medicine in accordance with declaration of Helsinki.

All subjects were subjected to the following:

Full history taking: Focusing on gestational age, postnatal age, sex, neurological symptoms such as seizures, perinatal maternal and fetal history, mode of delivery, APGAR scoring at 1 and 5 minutes and resuscitation steps.

Thorough clinical examination which included:

- General examinations.

- Vital signs and urine output.

- Anthropometric measurements: Weight

- Systemic examination

- Neurological examination

- Level of consciousness: Alert, lethargy or coma.

- Motor system: Power.

- Muscle tone and reflexes.

HIE staging system

HIE was defined as mild, moderate or severe using the Sarnat and Sarnat staging system [4]. The assessed elements included level of consciousness, muscle tone, tendon and complex reflexes, seizures, autonomic function and electroencephalogram (EEG) description.

Laboratory investigations: which were done for all subjects and included:

- CBC.

- Liver function tests.

- Serum electrolytes (Na, K, Ca).

- Arterial Blood gases (ABG): PH, PO2, PCO2 and Base excess.

- Serum creatinine: by routine technique.

Imaging techniques

- CT scan: which were done in all cases.

Collection of blood samples

3 ml of venous blood was taken from all studied groups, samples were centrifuged at 4000 rpm for 10 min; serum samples were separated and stored at -2°C to -80°C until assay.

Statistical Analysis

All data were analyzed using (SPSS version 20.0) software for analysis. According to the type of data, the following tests were used to test differences for significance. Differences between frequencies (qualitative variables) and percentages in groups were compared by Chi-square test. Differences between means (quantitative variables) in two parametric groups by t test, ROC curve for cut off, Kappa agreement to test the agreement. P value was set at <0.05 for significant results and <0.001 for high significant result [5].

Results

Table 1 summarized demographic data of the studied subjects. There was no significant difference between studied groups as regard gestational age and weight. There was also no significant difference between studied groups as regard sex. There was significant difference between studied groups as regard prenatal history of maternal hypertension and ante-partum hemorrhage. There was no significant difference between studied groups as regard mode of delivery. As regard Apgar score at 1 minute and 5 minutes of cases and controls, there was significant decrease in cases than in controls. As regard resuscitation steps among studied groups, the use of free oxygen flow and ETT were significantly increase in cases than in controls. Regarding clinical presentation of the studied neonates, they were classified according to Sarnat and Sarnat stages of HIE into stages I, II and III. Table 2 summarized the laboratory findings of the studied patients and controls including complete blood picture, ABG, serum electrolytes, liver enzymes, blood urea and serum creatinine. Table 3 showed comparison of serum creatinine level in studied patient subgroups according to Sarnat and Sarnat staging. This table showed that means of serum creatinine were significantly increased with the increase in severity of HIE according to Sarnat and Sarnat staging. Table 4 showed relation between serum creatinine and findings of CT brain among studied cases, there was statistically significant difference among serum creatinine levels regarding CT brain findings with marked elevation in serum creatinine which correlate with severity of HIE by CT brain.

      Group 1 (patients)
(n=36)
Group 2 (Controls)
(n=36)
Statistical test P value
Gestational age (weeks) Mean ± SD   38.27 ± 0.95 38.05 ± 1.05 0.66 0.5
Gender Male: No (%) 26 (72.2) 22 (61.1) 0.5 0.48
14 (38.9)
Female No (%) 10 (27.8) 12 (33.3%) 1.77 0.18
Mode of delivery NVD No (%) 28 (77.7%) 24 (66.7%)  
CS No (%) 8 (22.2%) 3.15 ± 0.36 0.12 0.89
Birth weight (Kg)   Mean ± SD 3.16 ± 0.47      
APGAR
score
at 1 min Mean ± SD 2.5 ± 0.51 6.3 ± 0.84 16.5 0.001*
at 5 min Mean ± SD 5 ± 0.87 8.7 ± 0.64 14.5 0.001*
Maternal risk factors Maternal  preeclampsia No (%) 10 (27.8%) 8 (22.2%) 1.59 0.02*
Maternal diabetes mellitus No (%) 8 (22.2%) 2 (5.6 %) 2.09 0.14
PROM No (%) 8 (22.2%) 2 (5.6 %) 1.12 0.28
Antepartum hemorrhage No (%) 10 (27.8%) 2 (5.6 %) 5.8 0.016*
Maternal risk factors Maternal renal failure No (%) 8 (22.2%) 0 (0%) 2.11 0.14
Sarnat and Sarnat Staging of HIE: Stage 1 No (%) 16 (44.4%) - - -
Stage 2 No (%) 12 (33.3%) -
Stage 3 No (%) 8 (22.2%) -
Resuscitation steps Free oxygen flow No (%) 0 (0 %) 14 (38.9 %) 8.69 0.003*
Assisted ventilation (Ambu bagging only) No (%) 16 (44.4%) 22 (61.1 %) 1 0.31
ETT No (%) 12 (33.3%) 0 (0%) 7.2 0.007
Chest compression No (%) 6 (16.7%) 0 (0%) 3.27 0.07
Medications No (%) 2 (5.6%) 0 (0%) 1.02 0.31
Impaired conscious level: Alert No (%) 22 (61.1%) 36 (100%) 0.3 0.1
Lethargy No (%) 8 (22.2%) 0 (0%) 5.09 0.00
Coma No (%) 6 (16.7%) 0 (0%) 2.4 0.00
Muscle Tone Normotonia No (%) 20 (55.6%) 36 (100%) 1.68 0.9
Hypotonia No (%) 12 (33.3%) 0 (0%) 9.8 0.00
Hypertonia No (%) 6 (16.1%) 0 (0%) 9.12 0.00
Tendon Reflexes Normal No (%) 24 (66.7%) 36 (100%) 0.27 0.7
Abnormal No (%) 12 (33.3%) 0 (0%) 9.5 0.00
Convulsions No convulsions No (%) 18 (50%) 36 (100%) 0.94 0.56
Tonic-clonic No (%) 12 (33.3%) 0 (0%) 17.9 0.001*
Subtle No (%) 6 (16.7%) 0 (0%) 10.4 0.001*

*P-value <0.05 significant.

Table 1: Demographic and clinical characteristics of the studied cases and the controls.

      Group 1 (patients)
(n=36)
Group 2 (Controls)
(n=36)
Statistical test P value
  WBCs Mean ± SD 14.7 ± 9.9 3.4 ± 1.6 5.09 0.001
  RBCs Mean ± SD 4.1 ± 1.3 5.2 ± 1.9 2.49 0.015
CBC HB Mean ± SD 12.7 ± 1.1 16.4 ± 1.5 1.4 0.14
Platelets Mean ± SD 193 ± 91.9 186.1 ± 60.5 0.3 0.76
ABG PH No (%) 7.03 ± 0.13 7.39 ± 0.03 11.2- 0.000*  
PCO2 (mmHg) No (%) 30.5 ± 12.7 39.2 ± 3.06 2.2 0.02
  PO2 (mmHg) Mean ± SD 39.5 ± 16.6 37.1 ± 6.5 7.8 0.001*
  HCO3 (mmol/L) Mean ± SD 11.1 ± 2.9 22 ± 2.1 12.5 0.001*
  BE (meq/L) Mean ± SD -11.1 ± 3.5 0.55 ± 0.23 3.9 0.35
Serum Ca Mean ± SD 0.99 ± 0.14 1.25 ± 0.07 11.28 0.001*
Serum Na Mean ± SD 129.6 ± 7.2 134.3 ± 6.3 2.4 0.016*
Serum K Mean ± SD 4.4 ± 0.75 4.5 ± 0.1 0.54 0.58
SGPT Mean ± SD 113.5 ± 114.2 21.1 ± 5.2 3.4 0.002*
SGOT Mean ± SD 110.2 ± 104.09 20.9 ± 5.06 3.6 0.001*
Serum Creatinine (mg/dl) Mean ± SD 0.87 ± 0.76 0.36 ± 0.21 2.7 0.01*
Blood urea (mg/dl) Mean ± SD 64.05 ± 22.7 27.16 ± 5.5 3.1 0.004*

*P-value <0.05 significant

Table 2: Laboratory characteristics of the studied cases and the controls.

  Sarnat I Sarnat II Sarnat III P.value
n=16 n=12 n=8
Serum creatinine (mg/dl) 0.51 ± 0.19 0.74 ± 0.25 1.3 ± 0.5 0.001

Table 3:  Comparison of serum creatinine level in studied patient subgroups according to Sarnat staging.

CT brain Serum creatinine At day 7 (mg/dl) t p-value
Mean ±SD    
Normal 0.44 ± 0.15 5.01 0.02
Brain odema 0.51 ± 0.01
Sever ischemia 0.73 ± 0.011

Table 4:  Comparison between serum creatinine in the studied patients according to findings of CT brain.

Discussion

Perinatal asphyxia is an insult to the fetus due to lack of oxygen (hypoxia) and/or lack of perfusion (ischemia) to various organs. It is associated with tissue lactic acidosis and hypercapnia. The effect of hypoxia and ischemia may not be identical, but they are difficult to separate clinically. Both factors probably contribute to injury [6].

Hypoxic-ischemic injury is the most important consequence of perinatal asphyxia [5].

Reperfusion of previously ischemic tissue may also promote the formation of excess oxygen free-radicals, which may damage cellular lipids, proteins, nucleic acid, and the blood brain barrier [7].

In response to acute hypoxia, the fetal neonatal cardiovascular system attempts to preserve blood flow to the brain, heart, kidney and adrenals. Multiple organs injury including acute kidney injury (AKI) occurs in 70% of HIE infants, and these must be some evidence of endorgan involvement to meet the definition of birth asphyxia [8].

Previously, it was unknown that the extent of systemic organ involvement might or might not correlate with the severity of encephalopathy. This can be transient and reversible. In fact, the CNS is often the main organ system that has residual sequelae at long term follow-up [9].

Many physiopathological mechanisms involved in the brain damage related to HIE of the newborn. Early assessment of the severity of an acute cerebral lesion secondary to hypoxia-ischemia may provide a very useful basis for preventive or therapeutic.

In our study, regarding brain CT scan, 24 (66.7℅) were normal, 4 (11.1℅) had brain odema and 8 (22.2℅) had sever ischemia.

Our study agreed with the observation made by Volpe that infants with normal CT scans rarely exhibit major neurological deficits on follow-up and infants with scans demonstrating marked diffuse hypodensity are rarely normal on follow-up [10].

Our study disagreed with findings of Tippin et al. [11]. Although CT scan may occasionally show early changes, it is most often normal hours after the insult and may remain unremarkable at later stages, even in patients with extensive neurological damage [12].

In our study, there was significant increase regarding blood urea and serum creatinine levels, in cases group when compared to control group (p<0.05). This results were in agreement with Huang et al. [13] who found that serum urea and creatinine level is significantly elevated in their HIE patient group in comparison to control group. Bhantnagar et al. reported also that the concentration of blood urea and creatinine were significantly higher in their hypoxic ischemic patients when compared to control group [14]. These findings were in accordance also with those of Gupta et al. who found that serum creatinine and blood urea were significantly higher in asphyxiated newborns compared to those of control group [15]. Our results were in accordance with many previously published articles including those of Gapal et al., Alaro et al., Amardiyanto et al. [16-18].

In this study, results of serum creatinine and blood urea were significantly correlated with the degree of hypoxic ischemic encephalopathy according to Sarnat and Sarnat as the level of serum creatinine in patient subgroups differ according to the Sarnat score. Sarnat stage I patients had a mean level of 0.51 ± 0.19 mg/dl. The mean level of serum creatinine for Sarnat II patients was 0.74 ± 0.25 mg/dl, whereas Sarnat III subgroup had a mean serum creatinine level of 1.3 ± 0.5 mg/dl.

These findings mean that urea and creatinine levels showed a highly significant increase with increased severity of Sarnat stages. These results were in accordance with Gupta et al. who were studying renal failure in asphyxiated neonates and stated that blood urea and serum creatinine were significantly higher in asphyxiated neonates when compared to the control group. A rising trend in the concentrations of blood urea and creatinine was also observed as HIE staging of neonates progressed, and the difference was statistically significant.

Andreoli, Gharehbaghi, Peirovifar, El-Gamasy and Nassar reported that HIE was one of the most prevalent risk factors for AKI in newly born infants [19-21].

In our study, there was significantly increase in serum creatinine in cases with abnormal CT findings when compared by those without brain abnormalities by CT brain and there was significantly increase in serum creatinine in cases with severe ischemia when compared by those with brain edema by CT brain.

Our results were in accordance with Park et al. who were studying the correlation between the severity of hypoxic ischemic encephalopathy and the development of acute renal failure in asphyxiated neonates, found that the greater the degree of HIE, the higher was the incidence of acute renal failure (ARF) [22].

Conclusions

Serum creatinine correlates with the severity of HIE as serum creatinine were significantly increased with the increase in severity of HIE according to Sarnat and Sarnat staging.

There was statistically significant difference among serum creatinine levels regarding brain CT findings with marked elevation in serum creatinine that correlate with severity of HIE by CT of brain. So higher serum creatinine levels was a bad prognostic marker for severity of HIE.

References

  1. Taniguchi H, Andrasson K (2008) The hypoxic ischemic encephalopathy model of perinatal ischemia. J Vis Exp 19: 3791-3955.
  2. Belet N, Belet U, Incesu L (2004) Hypoxic-ischemic encephalopathy: correlation of serial MRI outcome. Pediatr Neurol 31: 267-274.
  3. Neonatal Kidney Disease Improving Global Outcome (KDIGO): Proposed definition of AKI in Neonates.Kidnry International supplem (2016). Seminars in Fetal & Neonatal Medicine.
  4. Sangkae C, Jeffrey  M (2000) Perinatal hypoxic ischemic encephalopathy. Recent advances in pediatrics 18: 33-46.
  5. Kirkpatrick LA, Feeney BC (2013) A simple guide to IBM SPSS statistics for version 20.0. Student ed Belmont, Calif Wadsworth, Cengage Learning.
  6. Freeman JM, Nelson KB (2010) Intrapartum Asphyxia and cerebral palsy.Pediatrics 82: 240-249.
  7. Ashok K., Roopali M, Hari D (2008) Free radical injury and Blood Brain Barrier Permeability In Hypoxic-Ischemic Encephalopathy. Pediatrics 122: 722-727.
  8. Florio P, Marinoni E, Di Iorio R (2008) Urinary S100B protein concentrations are increased in intrauterine growth-retarded newborns. Pediatrics 118: 747-754.
  9. Shans P, Riphagen, S, Beyene J, Perlman M (2004) Multiorgan dysfunction in infants with post-asphyxial hypoxic ischemic encephalopathy. Archives of disease in childhood 89: 352-358.
  10. Volpe JJ (2008) Hypoxic –ischemic encephalopathy: biochemical and physiological aspects In : volpe JJ, ed. Neuology of the Newborn. Philadelphia PA: Elsevier Saunders 331-394.
  11. Tippin J, Adams HP, Smoker WR (1984) Early computed tomographic abnormalities following profound cerebral hypoxia. Arch Neurol 41: 1098-1100.
  12. Wijdicks EF, Campeau NG, Miller GM (2001) MR imaging in comatose survivors of cardiac resuscitation. AJNR Am J Neuroradiol 22: 1561-1565.
  13. Huang CC, Wang ST, Chang YC (1999) Measurement of the urinary lactate: creatinine ratio for the early identification of newborn infants at risk for hypoxic ischemic encephalopathy. New England J of Medicine 341: 328-335.
  14. Bhantnagar A, Bairwa AL, Meena KC (2014) Incidence of KI in perinatal asphyxia and its correlation with HIE staging. Indian J Res 3: 12-13.
  15. Gupta BD, Sharma P, Bagla J (2005) Renal Failure in Asphyxiated Neonates. Ind Pediatr 42: 928-934.
  16. Gopal G (2014) AKI in perinatal asphyxia. Indian J Pharm Biol Res 2: 60-65.
  17. Alaro D, Bashir A, Musoke R, Wanaiana L  (2014) Prevalence and outcomes of acute kidney injury in term neonates with perinatal asphyxia. Afr Health Sci 14: 682‑688.
  18. Amardiyanto R, Pudjiastuti P, Rundjan L, Pushponegoro HD (2013) Acute kidney injury in asphyxiated neonates. Paediatr Indones  53: 232‑238.
  19. Andreoli SP (2004) Acute renal failure in the newborn. Semin Perinatol 28: 112:123.
  20. Gharehbaghi MM, Peirovifar A (2007) Evaluating causes of acute renal failure in newborn infants. Pak J Med Sci 23: 877-880.
  21. Gamasy MA, Nassar MA (2017) Risk Factors for Acute Kidney Injury (AKI) in Newly Born Infants with Hypoxic Ischemic Encephalopathy (HIE). A Single Center Experience. International Journal of Research Studies in Medical and Health Sciences 2: 1-8 .
  22. Park SS, Chung SH, Song JH (2007) The correlation between the Severity of Hypoxic Ischemic Encephalopathy and the Develompent of Acute Renal Failure in Asphyxiated Neonates.J Kor soc Pediatr Nephrol 11: 32-40 .

Citation: El-Gamasy MA, Abdelmageed MM, Fakhreldin AR, Mehrez MM, Nassar MA, et al. (2018) Correlation of Renal Function with Severity of Hypoxic Ischemic Encephalopathy (HIE) in Egyptian Full Term Neonates. Neonat Pediatr Med 4: 157. DOI: 10.4172/2572-4983.1000157

Copyright: © 2018 El-Gamasy MA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Top