Approach to hypoglycemia in infants and children

Gandhi, Kajal

doi:10.21037/tp.2017.10.05

Cited by 40 publications

(31 citation statements)

References 85 publications

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“…Further research investigated other tissues such as skeletal muscle, which also can be profoundly affected by potentially life-threatening complications, such as rhabdomyolysis. Additional organ systems whose dysfunction generally is not life threatening are included in Table 2 [41][42][43][44][45][46][47][48][49][50][51][52]…”

Section: Clinical Manifestations Of Faodmentioning

confidence: 99%

“…• Signs of adrenergic symptoms and/or impairment of the nervous system, including lethargy, seizures, apnea, or coma [11,43,44] -CACTD Muscular • All FAOD [9] • Early childhood [45] • Myalgia (muscle pain) [15,26] • May present later in life provoked by endurance type activity, fasting, physiologic stress discharges from resting and plateau potentials [57]. Conduction velocities are slowed by a decrease in the presence of excitatory sodium current, leading to re-entry arrhythmia [57].…”

Section: Pathophysiologymentioning

confidence: 99%

“…The inability to break down fatty acids released from adipose tissue to replenish energy stores leads to a hypoglycemic state [3]. A key distinguishing characteristic of the form of hypoglycemia experienced by patients with FAOD is a lack of serum ketone bodies [43,64]. In neonates, the presentation of hypoketotic hypoglycemia secondary to FAOD can vary; however, it typically exhibits some signs of adrenergic stimulation and/or impairment of the central nervous system in the form of lethargy, seizures, apnea, or coma [11,43,44].…”

Section: Signs and Symptomsmentioning

confidence: 99%

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Clinical manifestations and management of fatty acid oxidation disorders

Merritt

MacLeod

Jurecka

et al. 2020

Rev Endocr Metab Disord

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Fatty acid oxidation disorders (FAOD) are a group of rare, autosomal recessive, metabolic disorders caused by variants of the genes for the enzymes and proteins involved in the transport and metabolism of fatty acids in the mitochondria. Those affected by FAOD are unable to convert fatty acids into tricarboxylic acid cycle intermediates such as acetyl-coenzyme A, resulting in decreased adenosine triphosphate and glucose for use as energy in a variety of high-energy–requiring organ systems. Signs and symptoms may manifest in infants but often also appear in adolescents or adults during times of increased metabolic demand, such as fasting, physiologic stress, and prolonged exercise. Patients with FAOD present with a highly heterogeneous clinical spectrum. The most common clinical presentations include hypoketotic hypoglycemia, liver dysfunction, cardiomyopathy, rhabdomyolysis, and skeletal myopathy, as well as peripheral neuropathy and retinopathy in some subtypes. Despite efforts to detect FAOD through newborn screening and manage patients early, symptom onset can be sudden and serious, even resulting in death. Therefore, it is critical to identify quickly and accurately the key signs and symptoms of patients with FAOD to manage metabolic decompensations and prevent serious comorbidities.

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Section: Clinical Manifestations Of Faodmentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

Section: Signs and Symptomsmentioning

confidence: 99%

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Clinical manifestations and management of fatty acid oxidation disorders

Merritt

MacLeod

Jurecka

et al. 2020

Rev Endocr Metab Disord

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“…Whipple's triad is useful in confirming hypoglycaemia: symptoms and/or signs consistent with hypoglycaemia, a documented low glucose concentration, and relief of signs/symptoms when plasma glucose concentration is restored to normal. However, young infants and children often cannot dependably recognize or communicate their symptoms, thus recognition of hypoglycaemia in this group may require confirmation by repeated glucose measurements and formal testing 134 …”

Section: Hypoglycaemia In Children Vs Adultsmentioning

confidence: 99%

Hypoglycaemia and its management in primary care setting

Ibrahim¹,

Baker

Cahn³

et al. 2020

Diabetes Metabolism Res

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Hypoglycaemia is common in patients with type 1 diabetes and type 2 diabetes and constitutes a major limiting factor in achieving glycaemic control among people with diabetes. While hypoglycaemia is defined as a blood glucose level under 70 mg/dL (3.9 mmol/L), symptoms may occur at higher blood glucose levels in individuals with poor glycaemic control. Severe hypoglycaemia is defined as an episode requiring the assistance of another person to actively administer carbohydrate, glucagon, or take other corrective actions to assure neurologic recovery. Hypoglycaemia is the most important safety outcome in clinical studies of glucose lowering agents. The American Diabetes Association Standards of Medical Care recommends that a management protocol for hypoglycaemia should be designed and implemented by every hospital, along with a clear prevention and treatment plan. A tailored approach, using clinical and pathophysiologic disease stratification, can help individualize glycaemic goals and promote new therapies to improve quality of life of patients. Data from recent large clinical trials reported low risk of hypoglycaemic events with the use of newer anti‐diabetic drugs. Increased hypoglycaemia risk is observed with the use of insulin and/or sulphonylureas. Vulnerable patients with T2D at dual risk of severe hypoglycaemia and cardiovascular outcomes show features of “frailty.” Many of such patients may be better treated by the use of GLP‐1 receptor agonists or SGLT2 inhibitors rather than insulin. Continuous glucose monitoring (CGM) should be considered for all individuals with increased risk for hypoglycaemia, impaired hypoglycaemia awareness, frequent nocturnal hypoglycaemia and with history of severe hypoglycaemia. Patients with impaired awareness of hypoglycaemia benefit from real‐time CGM. The diabetes educator is an invaluable resource and can devote the time needed to thoroughly educate the individual to reduce the risk of hypoglycaemia and integrate the information within the entire construct of diabetes self‐management. Conversations about hypoglycaemia facilitated by a healthcare professional may reduce the burden and fear of hypoglycaemia among patients with diabetes and their family members. Optimizing insulin doses and carbohydrate intake, in addition to a short warm up before or after the physical activity sessions may help avoiding hypoglycaemia. Several therapeutic considerations are important to reduce hypoglycaemia risk during pregnancy including administration of rapid‐acting insulin analogues rather than human insulin, pre‐conception initiation of insulin analogues, and immediate postpartum insulin dose reduction.

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“…A detailed history and physical examination along with relevant laboratory investigations are helpful in reaching the correct diagnosis. Broadly, the causes of hypoglycaemia in this age group include hyperinsulinaemic hypoglycaemia, hypopituitarism, adrenal insufficiency, ketotic hypoglycaemia of childhood, glycogen storage disorders (such as glucose-6-phosphatase deficiency), disorders of gluconeogenesis (such as fructose-1,6-diphosphatase deficiency), enzymatic defects (such as galactosaemia and hereditary fructose intolerance), defects of fatty acid oxidation, organic acidurias, sepsis and intoxication 2 3. Rarely, growth hormone deficiency (GHD) has been reported as a cause of recurrent hypoglycaemia either in isolation or combination with other metabolic defects 4…”

Section: Introductionmentioning

confidence: 99%

Isolated growth hormone deficiency presenting with recurrent hypoglycaemia in a toddler

Boro

Goyal²,

Khadgawat

2019

BMJ Case Rep

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Hypoglycaemia in infants and children is caused by a number of endocrine and metabolic defects, some of which are unique to this age group. Growth hormone deficiency (GHD) has been rarely reported as a cause of recurrent fasting hypoglycaemia in children. An 18-month-old male child presented to us for evaluation of neuroglycopenic symptoms caused by recurrent episodes of fasting hypoglycaemia. Laboratory evaluation revealed ketotic hypoinsulinaemic hypoglycaemia. The child was diagnosed to have GHD on the basis of two failed stimulation tests. A detailed work-up for metabolic and other hormonal causes of hypoglycaemia was negative. We present the case for its rarity and to highlight the importance of a detailed metabolic and hormonal assessment in evaluation of childhood hypoglycaemia.

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Approach to hypoglycemia in infants and children

Cited by 40 publications

References 85 publications

Clinical manifestations and management of fatty acid oxidation disorders

Clinical manifestations and management of fatty acid oxidation disorders

Hypoglycaemia and its management in primary care setting

Isolated growth hormone deficiency presenting with recurrent hypoglycaemia in a toddler

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