{"id":58487,"date":"2024-08-15T00:37:24","date_gmt":"2024-08-15T00:37:24","guid":{"rendered":"https:\/\/www.homeobook.com\/?p=58487"},"modified":"2024-08-15T00:37:24","modified_gmt":"2024-08-15T00:37:24","slug":"neonatal-hypoglycemia-clinical-insights-and-homoeopathic-approaches","status":"publish","type":"post","link":"https:\/\/www.homeobook.com\/neonatal-hypoglycemia-clinical-insights-and-homoeopathic-approaches\/","title":{"rendered":"Neonatal hypoglycemia : clinical insights and homoeopathic approaches"},"content":{"rendered":"

Dr Mehar Varghes<\/strong><\/p>\n

ABSTRACT
\nNeonatal hypoglycemia remains a critical concern in the care of newborns,presenting significant challenges in early detection and management.This condition,defined as low blood glucose levels in the first few days of life,can lead to neurologic impairment if not promply identified and treated.Management typically involves early detection through screening protocols,followed by interventions such as feeding,or glucagon administration if necessary.While conventional medicine provides established protocols for diagnosis and management.While homoeopathy offers individualised treatments tailored to symptoms.Homoeopathy presents an intriguing adjunctive therapy warranting research into its efficacy and safety.This article highlights on the definition,pathophysiology, etiology,Clinical features, investigations,and current management strategies underscoring the evolving role of homoeopathy in addressing neonatal hypoglycemia.<\/p>\n

Keywords<\/strong> : Neonatal Hypoglycemia,Hypoxic ischemic encephalitis, Keton bodies,Insulin<\/p>\n

INTRODUCTION
\nAs many as 5 to 15% of apparently healthy neonates suffer with neonatal hypoglycemia which is more common in nations with low resources. Low blood glucose levels are a common occurrence in the neonatal era and can be a significant cause of brain damage. Neonatal hypoglycemia occurs soon after birth as newborns adapt from continuous umbilical glucose to intermittent feeding. Hypoglycemia in neonatal period may be asymptomatic or severe and prolonged. In the neonatal population hypoglycemia may be associated with seizure activity and abnormal neurologic outcomes.Approximately half of the patients with newborn hypoglycemia\u00a0\u00a0 have hypoxic-ischemic encephalopathy (HIE). HIE might exacerbate the long-term brain damage brought on by hypoglycemia . Hence,neonatal hypoglycemia should always be given urgent attention.<\/p>\n

Treatment delays frequently lead to poor neurological outcomes .Despite limited evidence, concerns about severe neurologic consequences have driven the creation of screening guidelines to identify and manage neonates at risk for hypoglycemia, focusing on those with specific risk factors shortly after birth.According to recent research, using dextrose gel for treatment is both safe and effective, and it may even aid to promote breastfeeding.<\/p>\n

This article outlines pathophysiology of neonatal hypoglycaemia,discuss on the\u00a0 current dilemmas in clinical management,and describes some recent research that is beginning to indicate the potential for a more evidence-based approach to the diagnosis and treatment\u00a0 and outcome of neonatal hypoglycaemia.<\/p>\n

DEFINITION
\nIt is difficult to define hypoglycemia in neonates because of several reason. Over time, the definition of hypoglycemia has altered. In the 1960s, blood glucose (BG) values as low as 20 mg\/dL were considered acceptable; in the 1970s, levels as high as 40 mg\/dL were considered acceptable; and starting in 1988, many neonatologists began to accept BG concentrations as low as 47 mg\/dL (2.6 mmol\/L). Neonates of various gestation ages have variable maturity of nervous system and varable capacity to manifest the signs and symptoms of hypoglycemia.It is currently unknown what the crucial blood glucose level is\u00a0 necessary to maintain the integrity of newborn brain function.<\/p>\n

Low blood glucose levels, or hypoglycemia, are a screening test for neuroglycopenia or insufficient brain supply of glucose, and, in rare cases, an indication of an underlying endocrine or metabolic problem. However, hypoglycemia is not a diagnosis in and of itself. In the first 24 to 48 hours after birth, blood glucose levels in the healthy newborn population are typically lower than those in the populations of older children and adults.\u00a0 Hence, it is difficult to identify any particular levels of plasma glucose values that define pathologic hypoglycemia.<\/p>\n

PATHOPHYSIOLOGY
\nThe primary source of nutrition for the fetus is the transplacental transfer of nutrients, particularly glucose.A constant intravenous glucose supply is given to the fetus before to delivery. This glucose diffuses from the mother’s blood across the placenta through carrier-mediated facilitated diffusion hence, the blood glucose concentrations in the fetus are marginally lower than those in the mother. In a prenatal organism, endogenous glucose synthesis is not physiological.Even though the human fetus’s primary energy substrate is glucose, but a part of maternal glucose is converted by the placenta to lactate, which is released into the fetal and maternal circulation in 1:3 ratio<\/p>\n

Stress hormones including catecholamines and glucocorticoids are secreted during labor and delivery, which raises fetal blood glucose levels and frequently results in high cord blood glucose concentrations.After cord clamping, the abrupt cessation of the mother’s glucose supply causes a fast decrease in the blood glucose concentration of the newborn. The high rate of glycogenolysis leads to hastened depletion of hepatic glycogen stores, especially in preterm infants in which liver glycogen deposits are limited. The newborn brain has a 5\u201340 fold greater capacity to utilize ketone bodies than that of an infant or adult brain. Lactate appears to be important for neonates in the immediate postnatal life. Ketone bodies and lactate serve as important alternative fuels for maintaining cerebral energy supply of the brain.<\/p>\n

The exogenous glucose supply stops when the umbilical chord is severed, and blood glucose levels drop. A decrease in insulin production and an increase in counter-regulator hormones including glucagon, catecholamines, and glucocorticoids are the outcomes of this drop in blood glucose.These modifications work together to start the fetal body’s natural process of producing glucose through gluconeogenesis and glycogenolysis, which stabilizes blood glucose levels.Failure of this sequence of physiological changes can lead to hypoglycaemia, which is most common in the first few hours after birth.<\/p>\n

Transitional hypoglycemia, is temporary in most infants and usually recovers within a few hours to days. Fewer neonates have hypoglycemia that lasts for several days or weeks. Of these, some will develop permanent neonatal hyperinsulinism, which require further treatments.<\/p>\n

BRAIN INJURY AND GLUCOSE METABOLISM
\nThe brain relies on a regulated supply of glucose for energy, managed by glucose transporters like GLUT-1 and GLUT-3. Once glucose enters brain cells, it’s converted into glucose-6-phosphate, a step crucial for further energy production. This glucose is then directed into pathways like glycolysis, where it’s broken down to generate ATP, the cell’s energy currency.<\/p>\n

Excess glucose can be stored as glycogen, mainly in astrocytes within the brain, serving as a reserve energy source. When needed, glycogen can be broken down back into glucose-6-phosphate to fuel energy production.Brain function disruptions caused by hypoglycemia seem to initiate prior to any observable decline in overall brain ATP levels. Neuronal activity might be subdued as a means of conserving energy. ATP, produced through glycolysis under normal glucose levels (euglycemia), plays a key role in upholding glutamatergic neurotransmission.When blood glucose levels drop, cerebral blood flow initially increases to bolster glucose delivery to the brain.<\/p>\n

During the early metabolic shifts in hypoglycemia, the focus is on preserving cerebral energy levels by utilizing alternative fuels and starting glycogenolysis. Alongside lactate and ketone bodies, amino acids may serve as alternative substrates, as their concentrations decline notably alongside rising brain ammonia levels.Thus, even in the early stages of hypoglycemia, consciousness levels may decline despite relatively preserved ATP levels. This phenomenon can elucidate the discrepancy between cerebral energy metabolism and neuronal functions during hypoglycemia in certain instances.<\/p>\n

However, the newborn brain exhibits relative resilience to neuronal damage caused by hypoglycemia. This resilience may be attributed to lower cerebral energy requirements, increased cerebral blood flow during the initial phases of hypoglycemia, the neonatal brain’s enhanced capacity to utilize alternative fuels, and comparatively minor effects on the cardiovascular system due to ample endogenous carbohydrate reserves compared to adults.<\/p>\n

If\u00a0 hypoglycemia persists, cells experience an energy deficit. Under these circumstances, the energy-dependent Na+\/K+-ATPase fails, causing neurons to lose their capacity to uphold typical ionic gradients. Consequently, there are alterations in intracellular calcium and extracellular potassium concentrations ultimately lead to cellular damage.Continued hypoglycemia can lead to additional complications such as hypoxia, ischemia, and seizures, exacerbating the insult to the brain.<\/p>\n

Hypoglycemia often occurs alongside other health issues, resulting in distinct patterns of brain injury. Specifically, hypoglycemia triggers apoptotic cell death in oligodendrocyte precursor cells and impedes their maturation and myelination process. The consequences of hypoglycemic brain injury manifest as microcephaly, widened sulci, atrophic gyri, reduced cerebral white matter, and enlarged lateral ventricles.<\/p>\n

ETIOLOGY FOR NEONATAL HYPOGLYCEMIA
\nThe physiological reasons behind hypoglycemia in neonates encompass factors such as depleted hepatic glycogen reserves, insufficient muscle stores as a source of amino acids for gluconeogenesis, and inadequate lipid reserves for fatty acid utilization.<\/p>\n

Other serious causes of persistent Neonatal hypoglycemia include;<\/p>\n