Measuring the Risk: Hypoglycemia in Newborns of Diabetic Mothers-Cross Sectional Study

Introduction:

Neonatal hypoglycemia remains one of the most frequently encountered and clinically significant metabolic issues in newborns, particularly in those with identifiable risk factors. It results from the neonate’s immature ability to regulate blood glucose after separation from the maternal circulation. Since glucose is the brain’s primary energy source and neonatal brain metabolism is exceptionally high, inadequate glucose levels can result in serious consequences such as seizures, apnea, and long-term neurodevelopmental impairment if not promptly addressed.1

In utero, glucose is supplied by the mother through placental diffusion. After delivery, this supply stops abruptly, and the neonate must switch to internal mechanisms such as glycogenolysis and gluconeogenesis to maintain normoglycemia. While this transition is usually smooth in healthy term infants, complications can arise in high-risk groups like preterm infants, those with intrauterine growth restriction, and particularly infants of diabetic mothers (IDMs)¹.

IDMs are at heightened risk of hypoglycemia due to chronic exposure to maternal hyperglycemia during gestation. This leads to fetal pancreatic beta-cell hyperplasia and elevated insulin secretion—a state of fetal hyperinsulinemia—which continues postnatally and causes excessive glucose utilization and rapid depletion of circulating glucose². This predisposes IDMs to early-onset hypoglycemia, typically within the first few hours of life.

According to a review by Alemu et al., the global prevalence of neonatal hypoglycemia in IDMs ranges from 8% to 30%, with variation depending on diagnostic thresholds, timing of glucose measurement, maternal diabetes control, and neonatal monitoring protocols³. The review also emphasizes that despite extensive research globally, low- and middle-income countries often lack recent, region-specific data—highlighting the need for updated local studies to guide screening and intervention strategies³.

Although thresholds for defining neonatal hypoglycemia vary, most clinicians consider a plasma glucose level below 30 mg/dL (1.65 mmol/L) in the first 24 hours, or below 46 mg/dL (2.6 mmol/L) thereafter, to warrant clinical concern. Signs of hypoglycemia may be subtle—such as jitteriness, poor feeding, and lethargy—or severe, including apnea, cyanosis, seizures, or coma¹.

Chest Radiography:

 Assess cardiac size, shape, and great vessels carefully. In infants with macrosomia and a history of shoulder dystocia, clavicles should be examined for fractures both clinically and radiographically.

Abdominal, Pelvic, and Lower Extremity Radiography:

 Radiographs help identify skeletal defects in congenital malformations, particularly of the lower extremities.

Cardiac Echocardiography:

 IDMs are at higher risk for congenital heart defects such as ventricular septal defects (VSD) and transposition of the great arteries (TGA). Careful echocardiographic evaluation is essential to detect these abnormalities.

Barium Enema:

 Used to diagnose small left colon syndrome (“lazy colon”), which may mimic Hirschsprung disease. Diagnosis is confirmed by biopsy, showing normal ganglion cells in lazy colon but absence in Hirschsprung disease.

Vascular Access and Monitoring:

 Noninvasive monitoring (transcutaneous blood gases, pulse oximetry) reduces the need for invasive lines. However, indwelling lines (peripheral, umbilical, or central) are often necessary for continuous arterial pressure monitoring or when IV access is difficult, especially for administering high-concentration glucose infusions.

Histologic Findings:

In IDMs, pancreatic tissue typically shows enlarged and increased numbers of islets of Langerhans. Neonatal myocardium may exhibit cellular hyperplasia and hypertrophy, reflecting metabolic stress from maternal diabetes.

Figure1: An islet of Langerhans demonstrates insulitis with lymphocytic infiltrates in a patient developing type I diabetes mellitus. 

Management of Neonatal Hypoglycemia

Pharmacotherapy:

• Primary treatment: Glucose supplementation (e.g., intravenous dextrose).

• Other agents: Glucagon (including intranasal), inhibitors of insulin secretion such as diazoxide and octreotide, and rarely antineoplastic agents like streptozocin.

• Dietary therapy: Frequent feeding with complex carbohydrates is critical, especially for fasting or reactive hypoglycemia.

Electrolyte Management

• hypocalcemia and hypomagnesemia are common and should be monitored early.

• Magnesium must be corrected before calcium supplementation..

• Ionized calcium and magnesium levels are preferred for accurate assessment.

• Calcium gluconate supplementation (600–800 mg/kg/day) may be required, avoiding

Respiratory Management

Pulmonary Care:

 Respiratory support in infants of diabetic mothers (IDMs) is individualized according to clinical presentation. Oxygen therapy is used to maintain:

• Oxygen saturation >90%

• Transcutaneous oxygen tension between 40-70 mm Hg

• Arterial oxygen tension between 50-90 mm Hg

If the infant requires a fraction of inspired oxygen (FiO2) >40%, identifying the underlying cause of hypoxemia is crucial to guide specific treatment.

Assisted Ventilation:

 For severe respiratory distress, ventilatory support options include:

• Nasal continuous positive airway pressure (NCPAP)

• Endotracheal intubation with intermittent mandatory ventilation (IMV)

• Synchronized intermittent mandatory ventilation (SIMV)

Common indications for assisted ventilation are:

• FiO2 between 60-100% required to maintain arterial PO2 of 50-80 mm Hg

• Arterial PCO2 >60 mm Hg or rising by 10 mm Hg

• Apnea episodes

Criteria may vary based on the infant’s respiratory pathology and clinical condition.

Cardiac Management

Evaluation and Treatment:

 If congestive heart failure, cardiomegaly, hypotension, or a significant murmur is detected, echocardiography is essential to differentiate cardiac anomalies, septal hypertrophy, or cardiomyopathy. Management follows standard protocols for these conditions in neonates.

Special Considerations:

• Use cardiotonic agents cautiously in infants with hypertrophic cardiomyopathy or significant septal hypertrophy due to the risk of reduced left ventricular output.

• Beta blockers (e.g., propranolol) may be prescribed to alleviate outflow obstruction caused by septal hypertrophy.

Transfer, Consultations, and Follow-Up

NICU Transfer:

 IDMs with congenital anomalies, cardiac disease, or severe respiratory issues may need transfer to a tertiary-level neonatal intensive care unit (NICU) for advanced care and subspecialist involvement.

Consultations:

• Early pediatric cardiology consultation is often necessary due to the high incidence of cardiac abnormalities.

• Additional subspecialist referrals depend on the presence of other congenital defects or complications.

Outpatient Care:

 Routine well-baby care should be provided by a general pediatrician. Follow-up by specialists is tailored based on neonatal complications and their resolution.

Surgical Management

For fasting hypoglycemia caused by insulin-secreting tumors, surgical resection is the definitive treatment:

• Benign islet-cell adenomas have a high success rate after removal.

• Malignant islet-cell tumors have a success rate of approximately 50%.

Maternal glucose control during pregnancy and labor improves neonatal glucose regulation and reduces the need for IV glucose in infants.

Screening and Treatment Guidelines:

Neonatal blood glucose below 20–40 mg/dL within the first 24 hours is considered abnormal and requires intervention. Glucose should be monitored immediately after birth and at 30 minutes, 1, 2, 4, 8, and 12 hours, or if clinical signs appear. Intervention is needed if glucose remains below 36 mg/dL after feeding or if symptoms develop. If levels fall below 20–25 mg/dL, intravenous glucose is indicated, starting with a 2 mL/kg bolus of 10% dextrose over 5–10 minutes, followed by a continuous infusion at 6–8 mg/kg/min. Infusion rates should be adjusted to maintain glucose above 45 mg/dL. Central venous access may be needed for higher concentrations or volumes to avoid peripheral vein damage. Hydrocortisone may be required for persistent or Rapid diagnosis and treatment of hypoglycemia are critical regardless of the underlying cause.5

Diagnostic Criteria:

The hallmark diagnostic criteria, known as Whipple’s triad, include documented low blood glucose, the presence of symptoms consistent with hypoglycemia, and resolution of these symptoms once blood glucose levels normalize.Severe hypoglycemia.

● Laboratory investigations:

○ Serum insulin

○ Cortisol

○ Thyroid hormones

○ C-peptide

○ Proinsulin

Pathophysiology:

Hypoglycemic symptoms result from both sympathetic nervous system activation and brain glucose deprivation. Autonomic signs like sweating, tremors, and palpitations typically occur before neuroglycopenic symptoms such as confusion, irritability, and coma. The absolute glucose level, more than the rate of decline, triggers these symptoms. Recurrent hypoglycemia can lead to hypoglycemia unawareness, where warning signs diminish.4

A study by Zhong et al. found a U-shaped risk between HbA1c levels and hospitalizations for hypoglycemia in type 2 diabetes: both very low and very high HbA1c levels increased risk, especially in insulin users. The lowest risk occurred at an HbA1c near 7.0%. For HbA1c levels between 4.0–6.5%, each 0.5% rise reduced HH risk, whereas above 8.0%, the risk increased with higher HbA1c. Notably, this pattern was observed in insulin-treated individuals, but not in those on sulfonylureas³.5

Etiology of Hypoglycemia:

In individuals without diabetes, low blood sugar can arise from several non-drug-related causes. These include digestive system-related conditions, such as reactive hypoglycemia, which may occur following meals, particularly after bariatric procedures that accelerate stomach emptying and insulin release. Prolonged fasting is another possible cause, especially in people with reduced energy reserves or impaired ability to produce glucose. Hormonal disorders, including adrenal gland or pituitary dysfunction, can disrupt the body’s ability to respond to falling glucose levels. Additionally, liver diseases may impair glucose storage and synthesis, contributing to hypoglycemia. Rare genetic conditions, such as metabolic enzyme deficiencies, may also interfere with normal energy production. Proper identification of the cause is important to guide treatment and prevent recurrent episodes.6

Epidemiology of Hypoglycemia

The true prevalence of hypoglycemia in the general population remains difficult to determine, as nonspecific symptoms such as irritability and hunger are often attributed to low blood sugar without biochemical confirmation. 7 However, symptomatic hypoglycemia with glucose levels <50 mg/dL is estimated to occur in 5–10% of individuals presenting with relevant complaints. A Brazilian study by Lamounier et al. demonstrated a high frequency of hypoglycemic events in diabetic populations: 91.7% in patients with type 1 diabetes and 61.8% in those with type 2 diabetes over 4 weeks. Nocturnal and asymptomatic hypoglycemia were also prevalent, particularly in type 1 diabetics.8

Hypoglycemia is also a known complication of several medications, especially insulin and oral hypoglycemics, making it more common in diabetic than non-diabetic populations. Insulinomas, although rare (1–2 cases per million annually), represent a significant treatable etiology. Reactive hypoglycemia, most frequently reported in women aged 25–35, is typically benign and self-limiting.9

Epidemiology of Neonatal Hypoglycemia

In neonates, the incidence of symptomatic hypoglycemia ranges from 1.3 to 3 per 1000 live births in the United States, though figures vary depending on diagnostic criteria, feeding practices, and glucose assay methods. High-risk neonates—such as those who are large or small for gestational age (LGA/SGA), preterm, or born to diabetic mothers—exhibit significantly higher rates of hypoglycemia.

Inborn errors of metabolism, although rare, can also lead to persistent hypoglycemia in neonates. Reported incidences of specific metabolic disorders are as follows:

• Carbohydrate metabolism disorders: >1 in 10,000

• Fatty acid oxidation disorders: 1 in 10,000

• Hereditary fructose intolerance: 1 in 20,000–50,000

• Glycogen storage diseases: 1 in 25,000

• Galactosemia: 1 in 40,000

• Organic acidemias: 1 in 50,000

A Japanese study found that over 80% of NICU admissions among late preterm neonates (35–36 weeks of gestation) were due to hypoglycemia or apnea, highlighting the clinical burden in this age group.

Prognosis of Hypoglycemia

The prognosis of hypoglycemia is highly dependent on etiology, severity, and treatment timeliness. Acute, reversible causes (e.g., medication-induced or reactive hypoglycemia) typically confer a favorable prognosis with minimal long-term effects.4 In contrast, severe or prolonged episodes—particularly those involving CNS symptoms such as seizures or altered consciousness—can be life-threatening and may increase mortality in diabetic populations.10

Reactive hypoglycemia generally has a benign course and is managed effectively with dietary modifications. Meanwhile, studies such as that by Boucai et al. suggest that drug-induced hypoglycemia may be more reflective of underlying comorbid conditions rather than a direct cause of death.

Clinical Considerations in Neonatal Hypoglycemia

The initial evaluation of hypoglycemia necessitates a thorough medication, medical, and social history. Among neonates, screening is particularly warranted in those weighing <2 kg or >4 kg, LGA or SGA infants, preterm neonates (<37 weeks), those born to diabetic or septic mothers, and those with suggestive clinical features (e.g., jitteriness, apnea, hypotonia, seizures). .11

Hyperinsulinemic hypoglycemia, particularly transient neonatal hyperinsulinism, is common among infants of diabetic mothers (IDMs). These macrosomic infants often exhibit elevated insulin levels at the time of hypoglycemia and require increased feeding or glucose infusion.12 In cases of prolonged hyperinsulinism, characteristics include perinatal asphyxia, SGA status, or maternal toxemia.

Ketotic hypoglycemia, though rare, typically presents in children under age five following a prolonged fast, often with concurrent illness. These children may appear lethargic or comatose, with laboratory findings of marked hypoglycemia and ketonuria 13

Infants of Diabetic Mothers (IDMs)

IDMs are particularly vulnerable to hypoglycemia due to fetal hyperinsulinemia induced by maternal hyperglycemia. Specialized maternal-fetal care has dramatically reduced IDM-related morbidity and mortality, previously as high as 65%, to current rates below 5%. Nevertheless, approximately 3–10% of pregnancies are affected by glucose intolerance, the majority (80–88%) due to gestational diabetes.

Cesarean delivery is often required due to macrosomia-related risks such as shoulder dystocia. With optimal prenatal care, perinatal outcomes in IDMs can approximate those of non-diabetic pregnancies, excluding congenital defects.

Physical Examination

The clinical manifestations of hypoglycemia are nonspecific and can vary widely depending on the patient’s age, as well as the severity and duration of hypoglycemia. These findings are primarily due to either autonomic (adrenergic) activation or decreased availability of glucose to the central nervous system (CNS).14 Vital signs may reveal hypothermia, tachycardia (or bradycardia in neonates), hypertension, or tachypnea. In more severe cases, apnea, cyanosis, and respiratory distress may be evident, especially in neonates and young infants.15

On examination of the head, eyes, ears, nose, and throat (HEENT), patients may exhibit blurred vision, with pupils that are either normal or fixed and dilated. Icterus, typically of the cholestatic type, may be present and is often suggestive of hepatic involvement. Parotid tenderness may also be noted in cases of endocrine-related hypoglycemia.16 Cardiovascular assessment may cause fluctuations. 

Neurologic symptoms are often prominent and may include lethargy, confusion, fatigue, and loss of coordination. Some patients may present with an agitated or combative disposition, while others may lapse into a coma. Additional signs include seizures, tremors, diplopia, and manifestations resembling stroke syndromes.17 Respiratory involvement may present as dyspnea, tachypnea, or, in critical cases, acute pulmonary edema. Gastrointestinal findings are less specific but may involve nausea, vomiting, abdominal pain or cramping, and dyspepsia. The skin examination may reveal diaphoresis and warmth due to adrenergic stimulation, or signs of dehydration such as decreased skin turgor, particularly in prolonged or repeated episodes.18

In neonates and infants, who are unable to verbalize their symptoms, the clinical presentation can be subtle or severe. During the first 48 hours of life, neonates may be asymptomatic or exhibit life-threatening CNS and cardiopulmonary disturbances. Common signs in this population include poor feeding, hypotonia, apnea, cyanosis, lethargy, hypothermia, pallor, seizures, and tachycardia. Infants are particularly vulnerable to CNS injury due to glucose deprivation.19

Diagnostic Considerations

Because the consequences of untreated hypoglycemia can be devastating and the availability of effective treatment is immediate, diagnosis and management must be prompt in any patient suspected of hypoglycemia, regardless of the underlying cause.4 In patients with no prior history of hypoglycemia, a thorough workup is required to identify a potentially treatable disease. For individuals with diabetes, clinicians must consider recent changes in medications, physical activity, and the presence of infections. In some cases, particularly in the early stages of non–non-insulin-dependent diabetes, patients may experience postprandial hypoglycemia, which usually resolves spontaneously.20

The differential diagnosis of hypoglycemia is broad. Hepatic conditions such as hepatic failure, cirrhosis, galactose intolerance, fructose intolerance, and glycogen storage diseases can cause hypoglycemia. Endocrine disorders, including Addison’s disease, pheochromocytoma, glucagon deficiency, insulinomas, and extrahepatic tumors, must also be considered. Central nervous system disorders may present with symptoms mimicking hypoglycemia, including seizures or transient ischemic attacks. 21

Substance ingestion, including ethanol (particularly from sources like mouthwash or cologne in children), cocaine, salicylates, beta blockers, and pentamidine, can also result in hypoglycemia. Nutritional deficiencies such as prolonged fasting, protein-calorie malnutrition, renal disease, ketogenic diets, and metabolic disorders like L-leucine-sensitive hypoglycemia may be contributing factors.22 Autoimmune conditions, such as autoimmune hypoglycemia and Graves’ disease, should not be overlooked. Cardiac dysrhythmias may also be associated with hypoglycemic events. Additional etiologies include Jamaican vomiting sickness, post-surgical gastric dumping syndrome, excessive muscular activity, and diarrhea in children.

Given the wide spectrum of possible underlying causes, clinicians must approach each case of hypoglycemia with a broad differential, guided by clinical history, physical examination, and rapid laboratory evaluation. Early identification and management are crucial to prevent irreversible neurological damage and systemic complications.23

Differential Diagnosis of Hypoglycemia. 

Complications of Hypoglycemia (General and in Diabetic Therapy):

Hypoglycemia is a common complication of diabetes therapy, occurring in more than half of all patients undergoing treatment. Acute complications can include coma, seizures, hemiparesis, memory impairment, diminished language and cognitive abilities, ataxia, and cardiac dysrhythmias. QTc prolongation, particularly associated with sulfonylurea therapy, may increase the risk of arrhythmias, although a direct association with fatal arrhythmias in high cardiovascular risk patients has not been conclusively demonstrated. In critically ill patients, hypoglycemia is an independent risk factor for mortality, including cardiovascular and infection-related deaths. The risk of death increases with the severity of hypoglycemia. Long-term consequences of repeated or severe hypoglycemia include permanent neurological deficits and decreased quality of life. Non-severe hypoglycemic events, particularly in insulin-treated individuals, can significantly impair daily functioning, work performance, sleep, and emotional well-being.

Neonatal Complications in Infants of Diabetic Mothers (IDMs):

Infants of diabetic mothers are at high risk for a variety of complications. Metabolic abnormalities are prominent, particularly hypoglycemia, which may present within the first few hours of life and may persist for up to a week. It results from fetal pancreatic beta-cell hyperplasia due to chronic maternal-fetal hyperglycemia. Symptoms may include jitteriness, poor feeding, seizures, hypotonia, and apathy; Hypocalcemia and hypomagnesemia can also occur early and are associated with a delay in parathyroid hormone synthesis after birth. Abnormal iron metabolism, seen in approximately 65% of these infants, may predispose to neurodevelopmental delays due to iron redistribution during red blood cell breakdown 25

Hematologic complications such as polycythemia are common, arising from increased erythropoiesis due to chronic fetal hypoxia. This condition may manifest as a  sluggish capillary refill, or respiratory distress, and may increase the risk for stroke, necrotizing enterocolitis, seizures, and renal vein thrombosis. Thrombocytopenia may result from excessive erythroid precursor activity within the bone marrow. Hyperbilirubinemia, often secondary to polycythemia, is also frequently observed due to the increased burden on the neonatal liver to process the high red blood cell turnover.

Respiratory complications are frequent, with respiratory distress syndrome (RDS) and transient tachypnea occurring more commonly due to operative delivery and fetal macrosomia. Polycythemia can further contribute to respiratory complications such as persistent pulmonary hypertension of the newborn. Cardiovascular complications are notable, with up to 30% of IDMs developing cardiomyopathy. This may range from congestive heart failure due to a weak myocardium to significant septal hypertrophy and outflow tract obstruction. Echocardiography is often required to clarify the underlying cardiac issue in symptomatic infants.

In terms of growth, fetal macrosomia (birth weight >90th percentile) is a frequent finding, especially in the presence of late pregnancy maternal hyperglycemia. These infants often appear puffy, fat, and hypotonic. Conversely, impaired fetal growth resulting in small-for-gestational-age (SGA) infants may occur in up to 20% of diabetic pregnancies, most commonly due to maternal renovascular disease. This impaired growth is also linked with increased risks of perinatal asphyxia, which necessitates strong communication between obstetric and pediatric teams.

Congenital malformations are significantly increased in infants of diabetic mothers, particularly when maternal glucose control is poor during the first trimester. Central nervous system anomalies are notably more frequent, with the risk of anencephaly 13 times higher, spina bifida 20 times higher, and caudal dysplasia up to 600 times higher compared to infants of non-diabetic mothers. Neurological immaturity, such as poor sucking reflexes, has also been noted in infants of insulin-managed diabetic mothers. This may reflect abnormal brain metabolism and EEG patterns due to fetal hyperglycemia. Additionally, there is an increased incidence of renal anomalies (such as hydronephrosis and renal agenesis), ear malformations, gastrointestinal anomalies (such as duodenal or anorectal atresia and small left colon syndrome), and cardiovascular defects (including single umbilical artery, ventricular septal defects, atrial septal defects, transposition of the great arteries, coarctation of the aorta, and cardiomegaly).

Effective management of these complications relies heavily on preconception glycemic control in diabetic mothers, early identification and monitoring of high-risk infants, and robust communication between all members of the perinatal care team. Screening for hypoglycemia, hypocalcemia, and polycythemia in large-for-gestational-age or preterm infants is especially critical. Echocardiographic evaluation is often necessary in IDMs with cardiomegaly or poor perfusion to distinguish among potential causes.

Glucose metabolism:

Normal blood glucose levels are tightly regulated, typically maintained between 80–90 mg/dL

(4.4–5 mmol/L). After meals, glucose levels rise transiently to approximately 120–140 mg/dL (6.6–7.7 mmol/L), but efficient feedback mechanisms restore glucose concentrations to preprandial levels, usually within two hours of the last carbohydrate absorption.18

Insulin and glucagon are the primary hormones involved in this immediate feedback control system. Following a meal, elevated blood glucose stimulates increased insulin secretion, which promotes glucose uptake and storage in the liver as glycogen. Once glycogen stores in the liver and muscle are saturated, excess glucose is converted into fat for long-term energy storage. In contrast, when blood glucose levels decrease, glucagon secretion increases. Glucagon acts primarily on the liver to raise blood glucose by stimulating glycogenolysis and gluconeogenesis.

Normal hypoglycemic counterregulation. 

The Figure 1 above shows the body maintains blood glucose within a narrow range through a well-coordinated counterregulatory response to hypoglycemia. When blood glucose levels fall, insulin secretion decreases, and counterregulatory hormones—including glucagon, epinephrine, cortisol, and growth hormone—are released. Glucagon and epinephrine act quickly to stimulate hepatic glucose production via glycogenolysis and gluconeogenesis.4 Figure 1 shows that Cortisol and growth hormone provide a slower but sustained response by promoting gluconeogenesis and reducing peripheral glucose uptake. These mechanisms ensure adequate glucose delivery to critical organs, especially the brain, during periods of fasting or low glucose availability.

Hyperinsulinemia:

Congenital hyperinsulinism is usually due to abnormal beta-cell regulation or focal lesions like islet adenomas. It’s linked to genetic mutations in the sulfonylurea receptor (SUR) and beta-cell potassium ATP channel genes. Older terms like PHHI and nesidioblastosis are now replaced by specific genetic diagnoses.

Drug-induced hyperinsulinism results from hidden insulin use or accidental ingestion of oral hypoglycemics like sulfonylureas, especially in children. It can cause prolonged hypoglycemia. Low C-peptide levels help confirm exogenous insulin use. Diazoxide may be used to suppress insulin secretion in severe cases.

Approach Considerations:

 In recurrent hypoglycemia, initiate a 5% or 10% dextrose drip. Stabilize life-threatening conditions and start supportive care promptly. If the patient is alert with intact airway reflexes, give oral sugar-containing fluids (e.g., orange juice). In women with pregestational diabetes, maintaining intrapartum glucose between 4–7 mmol/L may help prevent neonatal hypoglycemia. Studies show mixed results for prophylactic dextrose gel use; while some suggest no benefit, others report reduced NICU admissions when used as adjunct therapy.

Emergency Department Care:

 Supportive care includes oxygen, IV access, and monitoring. Treat seizures not resolved by correcting hypoglycemia with anticonvulsants. Severe acidosis (pH <7.1) indicates underlying disease and should be addressed. Target glucose level: ≥45 mg/dL. If the infant cannot drink but has airway reflexes, use orogastric/nasogastric sugar solutions.

Data Collection Procedure:

 After ethical committee approval, neonates of diabetic mothers were enrolled via OPD and pediatric wards. Written consent was obtained. Maternal diabetes was confirmed through history and lab work. Neonatal glucose was assessed via 3 mL blood sample analyzed by experienced pathologists. Hypoglycemia was defined as glucose <46 mg/dL. Variables such as maternal age, newborn age, weight, diabetes type/duration were recorded. Strict exclusion criteria were applied.

Data Analysis:

Data was analyzed using SPSS v23. Mean ± SD was calculated for continuous variables; frequency and percentage for categorical variables. Stratification was used to control confounders. Post-stratification chi-square test was applied, with significance at p ≤ 0.05.

Note: Stratified analysis for hypoglycemia by maternal age, infant age, gender, duration of diabetes, and diabetes type is presented in Tables 8–13.

DISCUSSION:

Neonatal hypoglycemia is a common metabolic abnormality in newborns, primarily due to the inability to maintain glucose homeostasis. Glucose serves as a critical primary substrate for the brain, where its consumption is high; consequently, neurons and glial cells are particularly susceptible to the effects of hypoglycemia. Therefore, maintaining glucose homeostasis is essential for the overall physical and neurological development of newborns.

During gestation, maternal glucose is the sole source of glucose for the fetus, transferred via facilitated diffusion across the placenta following a maternal-to-fetal glucose concentration gradient. Hypoglycemia has been classified since 1937 into categories of “mild” (2.2 — 3.3 mmol/L), “moderate” (1.1 — 2.2 mmol/L), and “severe” (<1.1 mmol/L). However, there remains controversy regarding the precise plasma glucose level defining neonatal hypoglycemia. It is generally accepted that neonatal hypoglycemia is defined as a plasma glucose concentration below 30 mg/dL (1.65 mmol/L) within the first 24 hours of life. Despite advances, hypoglycemia remains a significant metabolic challenge in neonates.

In Table 2 study, the maternal age ranged between 18-40 years, with 35% of mothers aged 18-30 years and 65% aged 31-40 years (mean age 30 ± 10.71 years). Neonatal age distribution was 55% in the 1-15 days range and 45% in the 16-30 days range (mean age 15 ± 4.88 days). Table 3 shows Male infants comprised 58% of the cohort, and females 42%. Infant weights were predominantly between 3.5-4.5 kg (61%) and 4.6-6.5 kg (39%). Table 4 Duration of maternal diabetes was <5 years in 34% and >5 years in 66%. Table 5 The majority of mothers (88%) had type 1 diabetes, while 12% had type 2 diabetes.  Table 11 Neonatal hypoglycemia was present in 18% of infants, while 82% did not have hypoglycemia.

Table 3 shows Comparatively, Saqib et al. reported a mean neonatal age of 68.86 ± 34.39 minutes at blood sugar monitoring, with a mean gestational age of 38.25 ± 2.90 weeks and mean birth weight of 2844.3 ± 605 g. They found a hypoglycemia prevalence of 14.8%. Dim et al. emphasized that effective management of gestational diabetes mellitus (GDM) reduces perinatal morbidity and improves maternal quality of life. Postprandial glucose levels were noted to correlate better with adverse neonatal outcomes including hypoglycemia and macrosomia.

Barquiel et al. found that elevated third-trimester HbA1c and excessive gestational weight gain significantly increased neonatal complications including large-for-gestational-age (LGA) infants. Thomas et al. reported among 574 GDM mothers that 9.3% of neonates developed hypoglycemia, and a substantial proportion were LGA or preterm. In our study, 13.3% of births were preterm, and 14.8% of infants had hypoglycemia.

Flores-le Roux et al. observed that hypoglycemic infants were more frequently LGA, had lower umbilical pH, and were more often exposed to maternal hyperglycemia during labor, findings consistent with our results and other studies.

Graph given below is made from data we had collected, it has summarised all information.

CONCLUSION:

Our study concludes that the frequency of neonatal hypoglycemia in infants born to diabetic mothers is 18%. These findings emphasize the importance of close monitoring and management of blood glucose levels in neonates born to diabetic mothers to prevent adverse outcomes.

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