Severe Acidosis Research Articles

Perinatal antecedents of moderate and severe neonatal hypoxic ischaemic encephalopathy: An Australian birth cohort study.

Neonatal hypoxic ischaemic encephalopathy (HIE) is the most common cause of encephalopathy in the neonatal period and carries a high risk of mortality and long-term morbidity. The aim of this study was to investigate key antecedents of moderate and severe HIE in a large contemporary birth cohort. A retrospective cohort study of births meeting criteria was conducted between 2016 and 2020 at the Mater Mothers' Hospital, Brisbane, Australia. This is a quaternary perinatal centre and Australia's largest maternity hospital. Univariate and multivariate Firth logistic regression were used to account for imbalanced frequency classes between non-HIE and HIE groups. Maternal variables and intrapartum factors were investigated for associations with neonatal moderate and severe HIE. Overall, 133 of 46 041 (0.29%) infants were diagnosed with HIE: 77 (0.17%) with mild HIE and 56 (0.12%) with moderate/severe HIE. Nulliparity, type 1 diabetes mellitus and maternal intensive care unit admission were associated with increased odds of moderate/severe HIE. Intrapartum risk factors included emergency caesarean birth, emergency caesarean for non-reassuring fetal status or failure to process, intrapartum haemorrhage and an intrapartum sentinel event (shoulder dystocia, cord prolapse, uterine rupture and placental abruption). Neonatal risk factors included male sex, late preterm gestation (35+0 -36+6 weeks), Apgar score less than four at 5min, severe respiratory distress requiring ventilatory support and severe acidosis at birth. This cohort study identified a series of potentially modifiable maternal and obstetric risk factors for HIE. Risk factors for HIE do not appear to have changed significantly with evolution in modern obstetric care.

Severe lactic acidosis with euglycemic diabetic ketoacidosis due to metformin overdose.

Metformin-associated lactic acidosis is a well-known metformin treatment complication; however, the development of euglycemic diabetic ketoacidosis (euDKA) has rarely been reported. Here we report a case of lactic acidosis and euDKA after metformin overdose. A 57-year-old female patient was transferred to our hospital with severe metabolic acidosis and acute kidney injury. She had type 2 diabetes mellitus and was on oral antidiabetic therapy of vildagliptin metformin hydrochloride daily. On the admission day, she had committed suicide by overdosing 50 tablets of vildagliptin metformin hydrochloride, which was equivalent to 25,000mg of metformin and 2500mg of vildagliptin. She had severe lactic acidosis 5h after overdosing. However, after 34h of overdosing, serum lactate levels decreased while serum anion gap levels increased. She received single hemodialysis treatment. Serum total ketone bodies, β-hydroxybutyrate acetoacetic acid, and acetone were increased even after hemodialysis treatment. Her blood glucose levels have never exceeded 250mg/dL since admission. Therefore, we considered that the cause of metabolic acidosis in this patient was not only lactic acidosis but also euDKA. The causes of euDKA in our patient might be hepatic production of ketone bodies due to metformin overdose in addition to type 2 diabetes mellitus, starvation, infection, and stressful physical conditions such as vomiting and diarrhea. We propose that not only lactic acidosis but also ketoacidosis is one of the important pathological conditions in patients with metformin overdose.

Clinical profile and outcome of critically ill COVID-19 patients with diabetic ketoacidosis: A single-centre cross-sectional study in South India.

Clinical profile and outcome of critically ill COVID-19 patients with diabetic ketoacidosis: A single-centre cross-sectional study in South India.

Increased Use of Hyperosmolar Therapy for Suspected Clinically Apparent Brain Injury in Pediatric Patients with Diabetic Ketoacidosis during the Peak of the COVID-19 Pandemic.

The incidence of pediatric diabetic ketoacidosis (DKA) increased during the peak of the COVID-19 pandemic. The objective of this study was to investigate whether rates of hyperosmolar therapy administration for suspected clinically apparent brain injury (CABI) complicating DKA also increased during this period as compared to the three years immediately preceding the pandemic and to compare the characteristics of patients with suspected CABI before the pandemic, patients with suspected CABI during the peak of the pandemic, and those with DKA but without suspected CABI during the pandemic. Patients aged ≤18 years presenting with DKA before (March 11, 2017-March 10, 2020) and during the peak of the pandemic (March 11, 2020-March 10, 2021) were identified through a rigorous search of two databases. Predefined criteria were used to diagnose suspected CABI. Biochemical, clinical, and sociodemographic data were collected from a comprehensive review of the electronic medical record. The proportion of patients with DKA who received hyperosmolar therapy was significantly higher (P = 0.014) during the pandemic compared to the prepandemic period; however, this was only significant among patients with newly diagnosed diabetes. Both groups with suspected CABI had more severe acidosis, lower Glasgow Coma Scale scores, and longer hospital admissions (P< 0.001 for all) than cases without suspected CABI. During the pandemic, the blood urea nitrogen concentration was significantly higher in patients with suspected CABI than those without suspected CABI, suggesting they were more severely dehydrated. The clinical, biochemical, and sociodemographic characteristics of patients with suspected CABI were indistinguishable before and during the pandemic. In conclusion, administration of hyperosmolar therapy for suspected CABI was more common during the peak of the COVID-19 pandemic, possibly a result of delayed presentation, highlighting the need for increased awareness and early recognition of the signs and symptoms of diabetes and DKA, especially during future surges of highly transmissible infections.

Severe Metabolic Acidosis, Acute Renal Failure, and Delayed Paralysis Leading to Respiratory Depression due to Manganese ethylene-bis-dithiocarbamate.

Maneb is a widely used agricultural fungicide, which can lead to parkinsonism due to its neurotoxic effects on the dopaminergic system after chronic low-dose exposure. Previous acute human maneb poisoning cases occurred with low-dose maneb exposure through the dermal route causing renal failure. This report presents a case of acute renal failure and delayed paralysis due to ingestion of a large dose of maneb for a suicide attempt. A 16-year-old female patient was admitted to the emergency room because of drinking almost a whole bottle of maneb (400 mL [2 g L-1]) about 2 hours before. The patient was transferred to the intensive care unit with severe metabolic acidosis and renal failure. On the 4th day in intensive care unit, although the severe acidosis was resolved with haemodialysis, the patient was intubated because of ascending muscle weakness and dyspnoea. After staying in the intensive care unit for 9 days and in the nephrology ward for 2 weeks, the patient was discharged well from the hospital with no further need for haemodialysis but a persistent bilateral drop foot. One year after the event, renal functions were normal, and motor function in the lower extremities improved entirely.

Pediatric Extracorporeal Cardiopulmonary Resuscitation: Development of a Porcine Model and the Influence of Cardiopulmonary Resuscitation Duration on Brain Injury.

Background The primary objective was to develop a porcine model of prolonged (30 or 60 minutes) pediatric cardiopulmonary resuscitation (CPR) followed by 22- to 24-hour survival with extracorporeal life support, and secondarily to evaluate differences in neurologic injury. Methods and Results Ten-kilogram, 4-week-old female piglets were used. First, model development established the technique (n=8). Then, a pilot study was conducted (n=15). After 80% survival was achieved in the final 5 pilot animals, a proof-of-concept randomized study was completed (n=11). Shams (n=6) underwent anesthesia only. Severe neurological injury was determined by a composite score of mitochondrial function, neuropathology, and cerebral metabolism: scale of 0-6 (severe: >3). Among 15 piglets in the pilot study, overall survival was 10 (67%); of the final 5, overall survival was 4 (80%). Eleven piglets were then randomized to 60 (CPR60, n=5) or 30 minutes of CPR (CPR30, n=5); 1 animal was excluded from prerandomization for intra-abdominal hemorrhage (10/11, 91% survival). Three of 5 animals in the CPR60 group had severe neurological injury scores versus 1 of 5 in the CPR30 group (P=0.52). During ECMO, CPR60 animals had lower pH (CPR60: 7.4 [IQR 7.4-7.4] versus CPR30: 7.5 [IQR 7.4-7.5], P=0.022), higher lactate (CPR60: 6.8 [IQR 6.8-11] versus CPR30: 4.2 [IQR 4.1-4.3] mmol/L; P=0.012), and higher ICP (CPR60: 19.3 [IQR 11.7-29.3] versus CPR30: 7.9 [IQR 6.7-9.3] mm Hg; P=0.037). Both groups had greater mitochondrial injury than shams (CPR60: P<0.001; CPR30: P<0.001). CPR60 did not differ from CPR30 in mitochondrial respiration, neuropathology, or cerebral metabolism. Conclusions A pediatric porcine model of extracorporeal cardiopulmonary resuscitation after 60 and 30 minutes of CPR consistently resulted in 24-hour survival with more severe lactic acidosis in the 60-minute cohort.

Staying alert with polyhydramnios; an Ondine syndrome case

Abstract Objectives Amniotic fluid is essential for proper fetal development. In the case of severe polyhydramnios associated with low fetal growth, a number of different underlying disorders must be considered. One such condition is congenital central hypoventilation syndrome (CCHS) or Ondine’s curse, a rare genetic disease caused by mutation of the PHOX2B gene. The incidence of CCHS is estimated to be 1 case in 200,000 live births. No publications have been made to date on the intrauterine period findings. This precludes an early intrauterine diagnosis and impedes ethically responsible therapeutic options. Case presentation A 37-year-old patient presented in her second pregnancy with a small for gestation fetus and severe polyhydramnios evidenced in the third trimester ultrasound (US) study. There were no previous signs of maternal diabetes or fetal abnormalities at US. During the immediate postpartum period, the newborn presented repeated apneas with cyanosis and hypo-responsiveness. Neonatal arterial blood gas testing revealed severe respiratory acidosis requiring orotracheal intubation and admission to the Neonatal Intensive Care Unit. Over the following days, all imaging and functional test findings were within normal ranges. A de novo pathogenic PHOX2B variant was identified. Conclusions Despite a high mortality rate, no neurological sequelae or other systemic diseases were recorded, thanks to multidisciplinary and coordinated follow-up.

Duration of Invasive Mechanical Ventilation Post-Liver Transplantation: Does One Size Fit All?

Duration of Invasive Mechanical Ventilation Post-Liver Transplantation: Does One Size Fit All?

A typical phenotypes due to NDUFV1 mutations

Mitochondria have a critical role in energy metabolism, generating and scavenging of free radicals, intracellular Ca2+ regulation, and cell mitophagy. Dysfunction of the mitochondrial oxidative phosphorylation complex is the most frequent inborn errors of metabolism. Mitochondrial diseases are highly diverse in etiology, age of the disease onset, involvement of multiple organ systems, and genetic causes. NDUFV1 is a core subunit of mitochondrial Complex I (CI), and mutations cause CI deficiency. Clinically, CI deficiency is associated with severe infantile lactic acidosis, cardiomyopathy, encephalomyopathy, leukoencephalopathy, and Leigh syndrome. The cellular biology and molecular mechanisms of mitochondrial diseases are still elusive due to the heterogeneous genetic background and lack of phenotype-genotype correlation. Neurological abnormalities are the second most frequent presentations of mitochondrial diseases, including white matter abnormalities, psychomotor regression, and mental disability. The defects in myelin sheath or glial cells cause leukodystrophy which is a progressive genetical syndrome. To date, no therapy is available to cure mitochondrial diseases; exploration of the phenotype and molecular background are crucial for disease diagnosis, supportive treatments, proper genetic counselling, prenatal diagnosis, and experimental treatments. This article underscores the atypical clinical presentations of NDUFV1 mutations and the importance of a multidisciplinary approach to correlate phenotypes, biochemical, radiological, and molecular diagnosis. Implementation of multidisciplinary approach will enhance the possibility of discovering the therapeutic targets to treat mitochondrial disorders and ensure prenatal diagnosis to prevent inherited diseases.

Prenatal detection of aortic coarctation in a well-organized screening setting: Are we there yet?

We aimed to assess current prenatal detection rate (DR) of aortic coarctation (CoA) and its impact on neonatal outcome in the Netherlands to evaluate the efficacy of the Dutch screening protocol in which the cardiac four-chamber view, outflow tracts and three-vessel view are compulsory. All prenatally and postnatally diagnosed CoA cases between 2012 and 2021 were extracted from our PRECOR-registry. Annual DRs were calculated with a focus on the trend over time and attributing factors for detection. Postnatal outcome was compared between prenatally detected and undetected cases. 49/116 cases (42.2%) were detected prenatally. A higher chance of detection was found for cases with extracardiac malformations (71.4%; p=0.001) and the more severe cases with an aortic arch hypoplasia and/or ventricular septal defect (63.2%; p=0.001). Time-trend analysis showed no improvement in DR over time (p=0.33). Undetected cases presented with acute circulatory shock in 20.9% and were more likely to have severe lactic acidosis (p=0.02) and impaired cardiac function (p<0.001) before surgery. Even in a well-organized screening program, the DR of CoA still requires improvement, especially in isolated cases. The increased risk of severe lactic acidosis in undetected cases stresses the need for urgent additions to the current screening program, such as implementation of the three-vessel trachea view and measurement of outflow tracts.

Acute Exacerbation of Chronic Obstructive Pulmonary Disease – Clinical Presentation and Predictors of Outcome

Background and Objectives: Chronic Obstructive Pulmonary Disease (COPD) is a common, costly and preventable disease and is at present the fourth leading cause of death globally. To study the outcome of patients with acute exacerbation of COPD and to analyse the risk factors predicting adverse outcomes in patients with acute exacerbation of COPD. Patients and Methods: A Prospective study was conducted over a period of one year, from December 2021 to December 2022, Minimum of 50 patients, both male and female with AECOPD getting admitted to a Tertiary care centre were included in this study. Results: Of the 50 patients studied, 42 were males; all of them were smokers (84%). The mean age was 64.34 ± 10.47 years. The mean duration of the disease was 10.04±6 years. All patients presented with cough, recent worsening of Dyspnea and increased sputum purulence/volume. 70% patients had one or more associated co-morbid illness, majority had hypertension (40%). Of 32 patients with Respiratory failure on admission 17(53.12%) patients had Type II and 15(46.28%) had Type I failure. 44 patients received medical management and 6 patients required invasive mechanical ventilation (IMV). Overall mortality was 5 (10%). 20 variables were compared between survivors and non-survivors. Univariate sensitivity analysis revealed that presence of altered sensorium (P=0.001), Hypotension (P=0.02), cyanosis (P=0.00463), pedal edema (P=0.02), presence of infection (P=0.024) Severe Acidosis (P=0.012), Hypercapnia (P=0.016), cor pulmonale (P=0.04), at the time of admission and need for invasive mechanical ventilation (P&lt;0.001) as predictors of mortality. Conclusions: 64% of AECOPD presented with respiratory failure, majority were type II. Overall mortality was 10%. Altered Sensorium, pedal edema, presence of infection, cyanosis, hypotension, severe acidosis, hypercapnia and presence of cor pulmonale at the time of admission predict adverse outcome. Those who need invasive mechanical ventilation had high mortality. Survivors had less hospital stay.

Exertional rhabdomyolysis in a fallow deer (Cervus dama)

The aim of this report was to present a case of exertional rhabdomyolysis in a fallow deer. The diagnosis was made on the basis of clinical and blood laboratory findings. Despite the treatment, the outcome was fatal. Gross anatomy and histopathological examinations were performed, detecting degenerative changes in the heart, skeletal muscles, the kidneys and the liver. On the basis of ante and post mortem findings providing explanations of the pathophysiological mechanism of severe tissue damage - hypoxaemia, severe lactic acidosis, muscle rupture, electrolyte imbalance and renal block, it was concluded that all they have led to the death of the animal.

Twin Premature Infants With Riboflavin and Biotin Deficiency Presenting With Refractory Lactic Acidosis, Rash, and Multiorgan Failure During Prolonged Parenteral Nutrition.

We are reporting monochorionic, diamniotic twin premature infants born at 25 weeks and 6 days gestation with riboflavin (vitamin B2) and biotin (vitamin B7) deficiency, while on prolonged total parenteral nutrition (TPN) during vitamin shortage. They presented initially with skin rash, lactic acidosis, and thrombocytopenia. Both twins progressed to severe respiratory failure, severe lactic acidosis, with refractory vasodilatory shock, pancytopenia, ischemic bowel injury, acute kidney injury, liver injury, and capillary leak syndrome leading to death of twin A. The surviving twin B was diagnosed with riboflavin and biotin deficiency that presented with abnormal metabolic work up suggestive of maple syrup urine disease, glutaric acidemia type 2, and X-linked adrenoleukodystrophy. Twin B was started on riboflavin and biotin supplementation at 41 days of life, with rapid improvement in clinical findings and laboratory abnormalities within days of starting biotin and riboflavin supplementation. He was discharged home in stable condition at 49 weeks of postmenstrual age.

Severe lactic acidosis after re-exposure to linezolid in a person living with HIV and multidrug resistant tuberculosis: a case report

Abstract Linezolid-induced lactic acidosis is rare and portends a poor prognosis. The mechanism of toxicity may be related to inhibition of mitochondrial ribosomes. We present the first case in the literature of a patient with HIV and multidrug resistant tuberculosis with fatal lactic acidosis secondary to linezolid re-exposure. The index case relates to a 37-year-old lady with a background medical history of HIV, on fixed combination antiretroviral therapy. In addition, she had multidrug resistant pulmonary tuberculosis and was being treated on a salvage antituberculosis regimen containing linezolid. She presented with a 1-day history of backpain, nausea and vomiting. Clinically she was severely acidotic with a lactate of 12 mmol/L, which peaked at 19 mmol/L. A presumptive diagnosis of lactic acidosis was made based on the history and exclusion of other causes. The patient demised despite management in the intensive care unit with continuous veno-venous haemodialysis (CVVH) and mechanical ventilation. The diagnosis of linezolid-induced lactic acidosis requires a high index of suspicion and exclusion of other causes. In the absence of definitive treatment, early diagnosis, drug discontinuation and prompt supportive management including continuous veno-venous haemodiafiltration are key in helping to reduce the high mortality associated with this toxicity.

A case of an ischemic bulky free flap contributing to severe postoperative lactic acidosis following major head and neck reconstructive surgery

A case of an ischemic bulky free flap contributing to severe postoperative lactic acidosis following major head and neck reconstructive surgery

Euglycemic Diabetic Ketoacidosis Related to SGLT2 Inhibitor Use in a Patient With Cobalamin C Deficiency and Diabetes

A 24-year-old woman with cobalamin C deficiency (CblCD), autoimmune thyroiditis, and recently diagnosed diabetes mellitus presented with weight loss, emesis, and abdominal pain. She had been placed on sodium-glucose cotransporter inhibitor (SGLT2i) therapy because of metformin intolerance, with the addition of a dipeptidyl peptidase-4 inhibitor. Biochemical analyses demonstrated severe acidosis, initially attributed to CblC-associated metabolic decompensation. Subsequent evaluation led to the diagnosis of SGLT2i-induced euglycemic diabetic ketoacidosis in a patient with type 1 diabetes mellitus. This case highlights the importance of assessing for insulin deficiency when evaluating acidosis and the management challenges of common diseases in adults with inherited metabolic disorders.

Amitraz poisoning – A rare and uncommon case of poisoning and its management

A 25-year-old male presented to the peripheral hospital with an alleged history of ingestion of amitraz toxin 12.5% (approximately 150 mL), and presented with complaints of nausea, vomiting, abdominal pain, and weakness. On examination, he was conscious but disoriented and agitated, oxygen saturation (SpO2) was 89%–90% on room air, pulse rate was 40/min, blood pressure (BP) was 110/70 mmHg, and bilateral (B/L) crepitations were present on auscultation. Emergency treatment included – intravenous(IV) fluid, atropine 0.6 mg IV, and gastric lavage. Oxygen was given through an oxygen mask with a reservoir bag at 10 L/min. After some time, the patient's Glasgow Coma Scale (GCS) started deteriorating, and arterial blood gas (ABG) analysis revealed severe acidosis with pH of 7.109, pCO2 – 73, and HCO3 – 23.1, and immediately, the patient was transferred to a higher center given falling GCS, decreased saturation, and ABG finding. On presentation in the emergency department in our tertiary care center, the patient was unconscious, SpO2 was 69% on oxygen nonrebreathing mask – NRBM Mask at 15 L, BP was 128/78 mmHg, pulse rate was 104/min, and B/L crepitations were present on auscultation. The patient was immediately intubated in casualty and shifted to the intensive care unit for further management. Amitraz is a triazapentadiene, 1,5 di (2,4 dimethylphenyl) 3 methyl 1,3,5 triaza penta 1,4 diene, a formamidine pesticide, α2 adrenergic agonist in the central nervous system belongs to the amidine chemical family. The systemic effect of amitraz toxin is due to the activation of the pure α2-adrenergic agonist. It is a rare kind of poisoning in humans, and there exists a paucity of literature on the management of the aforementioned poisoning. Only a limited number of case reports of human intoxication have been published and most of them are of accidental ingestion by children. Due to insubstantial data on its management, this case report will be advantageous for practitioners working in emergency and intensive care departments.

A Novel Mutation in the OXCT1 Gene Causing Succinyl-CoA:3-Ketoacid CoA Transferase (SCOT) Deficiency Starting with Neurologic Manifestations.

Succinyl-CoA:3-oxoacid CoA-transferase (SCOT) deficiency is an inborn error of ketone body utilization characterized by intermittent ketoacidosis crises. This study reports the first Iranian patient with SCOT deficiency who presented with seizure and hypotonia at birth. Accordingly, she was consequently re-hospitalized due to hypotonia and respiratory distress. Laboratory tests revealed hyperammonemia, ketonuria, and metabolic acidosis. Besides, the plasma glucose level was normal without any other abnormality. Despite treatment with high-dose bicarbonate, severe acidosis persisted. Poor response to treatment raised a significant diagnostic challenge among specialists until genetic investigation identified a homozygous nonsense mutation (c.79G>T; p.Gly27*) in the OXCT1 gene (NM_000436), causing SCOT deficiency. Genetic studies help clinicians achieve a definite diagnosis of such metabolic disorders. In this case, the accurate and early diagnosis of SCOT deficiency opened new therapeutic possibilities, including frequent carbohydrate-rich meals and low fat and protein diet. Moreover, our findings expand the mutational and clinical spectrum of SCOT deficiency.

Correlation of cord Blood pH with Nucleated RBC and Serum LDH in Neonates with Perinatal Asphyxia

Introduction: Perinatal asphyxia is one of the leading causes of neonatal mortality in developing countries. No single indicator has good diagnostic efficacy for perinatal asphyxia and only a combination of various indices may help in diagnosis. This study aims at determining the utility of serum lactate dehydrogenase (LDH) and cord blood nucleated red blood cell (nRBC) count as surrogate markers to pH in perinatal asphyxia. Methods: It is an observational study done over a period of 18 months. All newborn babies fitting into inclusion criteria were enrolled into the study. After initial resuscitation, cord blood was sent for pH and nRBC analysis and serum LDH levels was estimated from first collected blood sample (within six hours). Data was collected on excel sheet, Pearson’s correlation coefficients and ROC curves were used to tabulate results. Results: Our study included 74 neonates with perinatal asphyxia. Mean pH was 6.99 (SD - 0.138). Mean nRBC count was 38 / 100 WBC (SD17.9) and mean LDH level was 1478 IU / L (SD - 429). Cord blood pH showed significant (p &lt; 0.001) correlation with raising nRBC count and LDH levels ROC plot showed nRBC count (AUC: 0.7866) and Serum LDH (AUC: 0.8143) as very good predictors of severe acidosis in perinatal asphyxia. Conclusions: Cord blood nRBC count and serum LDH levels are significantly increased in perinatal asphyxia and correlate well with severity of acidosis. Nucleated RBC count and serum LDH can be used as surrogate markers to diagnose perinatal asphyxia.

Evaluation and Neurodevelopmental Outcomes of Infants with Hypoxic Ischemic Encephalopathy Treated with Therapeutic Hypothermia: A Single Center Experience

Hypoxic ischemic encephalopathy (HIE) is an important cause of mortality and morbidity in newborns. Our study aimed to determine the neurodevelopmental outcomes, risk factors, and the relationship between risk factors and prognosis of cases followed up with HIE diagnosis and who were treated with hypothermia treatment. Medical records of 23 patients who were followed up with HIE diagnosis in the pediatric neurology outpatient clinic between January 1, 2018, and December 31, 2021, and treated with therapeutic hypothermia in the newborn period were retrospectively reviewed. Denver Developmental Screening Test II was used in the developmental evaluation. Neurodevelopment was normal in 12 (52.2%) of 23 cases and retarded for age in 11 (47.8%) cases. Variables such as Sarnat encephalopathy score in the neonatal period, need for prolonged ventilation, presence of severe acidosis at birth, Apgar scores at the 1st and 5th minutes, and abnormal cranial magnetic resonance (Mrg) findings were determined to be major factors in determining neurodevelopmental prognosis in asphyxic cases. The male gender was found to be riskier in terms of prognosis. Of the patients with HIE, retardation was determined for fine motor skills in 52.2%, speaking in 39.1%, gross motor skills in 26.1%, and personal development in 21.7%. Epilepsy, cerebral palsy, and speech disorders were the most common chronic period problems in patients with HIE. Despite therapeutic hypothermia treatment, neurodevelopmental problems are still observed in newborns with HIE. We found that male gender, low Apgar score, severe acidosis, and abnormal cranial Mrg findings in the neonatal period are risk factors in determining the neurodevelopmental prognosis of newborns with HIE. Monitoring and supporting the development of HIE cases with risk factors from the first months of life and intervening in developmental problems promptly are crucial in order to improve long-term outcomes.