Download Free Medical Neonatal Hypoglycemia And Hypocalcemia PowerPoint Presentation

Neonatal Hypoglycemia And Hypocalcemia PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Neonatal hypoglycemia and hypocalcemia” by Dr V Sowjanya Bhanu.

This medical PowerPoint presentation is about neonatal hypoglycemia and hypocalcemia, two common conditions that affect newborns. Hypoglycemia refers to low blood sugar levels, while hypocalcemia refers to low levels of calcium in the blood. These conditions can occur separately or together and can cause a range of symptoms and complications if left untreated.

Neonatal Hypoglycemia-Neonatal hypoglycemia occurs when a newborns blood sugar levels are too low. This can happen for a variety of reasons, including prematurity, maternal diabetes, intrauterine growth restriction, and excessive insulin production by the babys pancreas. Symptoms of neonatal hypoglycemia can include jitteriness, lethargy, poor feeding, and seizures.

Treatment for neonatal hypoglycemia involves frequent feeding to help stabilize the babys blood sugar levels. If this is not enough, intravenous glucose may be given to the baby to raise their blood sugar levels. In some cases, hospitalization may be necessary to monitor the babys blood sugar levels and ensure they are stable.

Neonatal Hypocalcemia-Neonatal hypocalcemia occurs when a newborns blood calcium levels are too low. This can happen for a variety of reasons, including prematurity, maternal hypoparathyroidism, and certain medications given to the mother during pregnancy. Symptoms of neonatal hypocalcemia can include jitteriness, muscle twitching, and seizures.

Treatment for neonatal hypocalcemia involves giving the baby calcium supplements, either orally or through an IV. If the baby is not able to absorb calcium properly, other medications may be given to help improve calcium absorption. In some cases, hospitalization may be necessary to monitor the babys calcium levels and ensure they are stable.

It is important for newborns to be monitored for both hypoglycemia and hypocalcemia, especially if they have risk factors for these conditions. Early detection and treatment can help prevent complications and ensure the best possible outcome for the baby.

Tags : Neonatal hypoglycemia, hypocalcemia, Neonatal-Perinatal Medicine, Neonatal-Perinatal Medicine PowerPoint presentation

Published on : Jun 07, 2023 | Views : 768 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

NEONATAL HYPOGLYCEMIA AND HYPOCALCEMIA Dr v sowjanya Bhanu Senior resident
Slide 2-

Introduction Hypoglycemia is one of most common metabolic problem in neonates. Persistent hypoglycemia is most likely associated with endocrine disorders and possible neurologic sequelae
Slide 3-

Physiology Glucose provides 60-70% of energy to fetus and newborn. Fetal glucose is approximately 2/3 of maternal levels.(Trans placental facilitated diffusion) Why prone to develop hypoglycemia:- 1.Umblical cord cutting at birth. 2. Inadequate storage of glycogen. 3. Immature adaptive mechanisms. 4. Prone to long term neurological damage.
Slide 4-

Lowest value upto 25-40 mg/dl in the first 1 - 2 hours of life. Stabilize by 65-70 mg/dl by 3-4 hours of age spontaneously or with feed/intervention
Slide 5-

Epidemiology Incidence: 1.3-3/1000 live birth. Incidence varies with definition, population, method, timing of feed and type of glucose estimation method. Plasma value is 10-15% higher than blood glucose value. Incidence is higher in at risk neonates (LPT>SGA>IDM>LGA)
Slide 6-

DEFINITION Clinical definition:- Based on symptoms associated with hypoglycemia and resolution of symptoms when glucose restored in normal range. Sometimes development of signs and symptoms may be late.
Slide 7-

Operational Threshold of cornbalth: Glucose level at which intervention should be considered. It is an indication of action not diagnostic of disease or abnormality. It is based on clinical experience and analysis of available evidences.
Slide 8-

Healthy term: <24 hrs: 30-35 mg/dl at one time 45mg/dl if persist after feeding or recurs. >24 hrs: 45-50 mg/dl Symptomatic: 45 mg/dl Asymptomatic with risk factor: 36 mg/dl Any baby with <20-25 mg/dl
Slide 9-

Indications for routine screening LBW infants(<2.5 kg) Preterm (<35 weeks) SGA (BW<10th centile),L G A, I D M Rh hemolytic disease Post exchange transfusion Infants on TPN Sick neonates(sepsis, shock, asphyxia, polycythemia, distress etc.) Mother receiving terbutaline, labetalol, oral hypoglycemics
Slide 10-

Screening schedule Category of infants At risk neonates Sick infants Stable VLBW4. infants on TPN IDM Exchange transfusion Time schedule At 2, 6, 12, 24, 48, 72hrs Every 6-8 hrly Initial 72 hr : 6-8 hrly After 72 hrs: Once a day At 1, 2, 3, 6, 12, 24,26 and 48 hrs 1 hr after exchange
Slide 11-

ETIOLOGY Hyperinsulinemic hypoglycemia: Major cause of persistent and recurrent hypoglycemia IDM: historically known mc cause Congenital/genetic: Mutation of pancreatic beta cell ATP sensitive K+ channel . (ABCC8,KCNJ11 Encodes for SUR1,Kir )
Slide 12-

Birth asphyxia, Development syndromes- Beckwith-wiedemann syndrome Erythroblastosis Maternal tocolytic drugs Malpositioned umbilical artery catheter Abrupt cessation of high glucose infusion. After exchange transfusion with high BG concentration. Insulin producing tumors eg. nesidioblastosis, islet cell adenoma or dysmaturity.
Slide 13-

Decreased Production/Stores Prematurity IUGR Inadequate caloric intake Delayed onset of feeding
Slide 14-

Increased Utilization or decreased production Peri-natal stress Exchange transfusion (reactive hypoglycemia Endocrine deficiency Defect in carbohydrate and AA metabolism Polycythemia Maternal therapy with beta blocker causes prevention of sympathetic stimulation of glycogenolysis
Slide 15-

DIAGNOSIS SYMPTOMS: Irritability Tremors Jitteriness Exaggerated Moros reflex Seizures,high pitched cry Lethargy,hypotonia,cyanosis Poor feeding
Slide 16-

METHODS OF BGL ESTIMATION Reagent strips/ Glucometer:- Most widely used method, mainly used for screening Measures whole blood glucose level which is 15% lower than plasma value. Unreliable at the lower values. Capillary samples ( Heel prick).
Slide 17-

Glucose oxidase (colorimetric) method:- Used in laboratories Most reliable and accurate method Glucose electrode ( Blood gas analyser):- Minimal volume of blood required
Slide 18-

MANAGEMENT Goal of current management is to anticipate a n d prevent hypoglycemia rather than treatment. Asymptomatic:-BGL 20-45 mg/dl: Trial of feed and repeat BGL after 1 hr If repeat BGL >45, 2 hrly feed with 6 hrly BGL for 48 hrs. If repeat BGL <45, confirm with lab report and management is as for symptomatic hypoglycemia
Slide 19-

BGL <20 mg/dl: Start treatment with IV glucose Goal: >45 in first 24 hr and >50 thereafter.
Slide 20-

Symptomatic Urgent treatment: 2 ml/kg of 10% D/W (200mg/kg) over 1 minute Continuing therapy: Start GIR @6-8 mg/kg/min
Slide 21-

Recheck BGL 15-30 minute after bolus, then hrly until stable Additional bolus of 2 ml/kg may be needed If BGL is stable & in normal range, feeding may be started & GIR may be tapered.
Slide 22-

Refractory and prolonged hypoglycemia Refractory: GIR requirement of >12 mg/kg/min for >24 hrs. Prolonged/Persistent: Unstable BGL beyond 5 – 7 days. Causes:- Hyperinsulinemic hypoglycemia Congenital hypopituitarism, hypothalamic deficiency Adrenal insufficiency, epinephrine deficiency GSD, galactosemia, fructose intolenrance Defects in AA metabolism eg-MSUD, tyrosinemia Polycythemia
Slide 23-

Critical lab sample: Evaluation requires drawing blood for insulin ,cortisol,aminoacids when glucose levelis <40mg/dl Glucose Insulin (>2 micro U/ml diagnostic) I:G ratio during hypoglycemia >0.3-0.5 Beta hydroxy butyrate and FFA levels Cortisol: to screen the integrity of HPA axis
Slide 24-

If insulin level is normal for blood glucose consider additional testing: GH, ACTH, T4 &TSH, Glucagon, Cortisol Plasma AA, Blood NH3, Blood lactate level Urine ketones, reducing substance, AA, organic acids Genetic testing for mutations 18F fluoro L-DOPA PET scan to identify focal lesion in pancreas to consider for subtotal pancreatectomy.
Slide 25-

Management AIMS Protocol
Slide 26-

Treatment Hydrocortisone: 5 mg/kg/day iv q 12 hrly ↓Peripheral glucose utilization, ↑gluconeogenesis and effect of glucagon. Glucagon: 0.025-0.2 mg/kg iv/im/sc. Max- 1 mg. Increase glucose release Temporary measure and can be used in infants with good glycogen stores. Diazoxide: 5-8 mg/kg/day q 8-12 hrly. Inhibit insulin release Octreotide: 5-20 mcg/kg/day iv/sc q 6-8 hrly. Inhibit insulin secretion, can be used when diazoxide does not successfully control BGL. Subtotal pancreatectomy
Slide 27-

Long term follow up and evaluation MRI Scan : Typical pattern of CNS injury particularly in parieto-occipital cortex and sub cortical white matter. Neonates have developmental delay, cerebral palsy, motor impairment, blindness and hearing impairement.. Babies who have had symptomatic hypoglycemia should have close follow up at 3, 6, 9, 12 & 18 month age for growth, neurodevelopment, vision and hearing loss.
Slide 28-

HYPOCALCEMIA DEFINITION: Hypocalcemia is defined as total serum calcium of less than 7 mg/dL (1.75 mmol/L) or ionized calcium less than 4 mg/dL (1 mmol/L) In very low birth weight infants the ionised calcium levels of 0.8 to 1mmol/lit are common and not usually associated with clinical symptoms
Slide 29-

TYPES OF NEONATAL HYPOCALCEMIA The early onset hypocalcemia: presents within 72 h requires treatment with calcium supplementation for at least 72 h. late onset hypocalcemia: usually presents after 7 days and requires longer term therapy.
Slide 30-

CAUSES OF EARLY ONSET HYPOCALCEMIA Prematurity Preeclampsia Infant of Diabetic mother Perinatal stress/ asphyxia Maternal intake of anticonvulsants (phenobarbitone, phenytoin sodium) Maternal hyperparathyroidism Iatrogenic (alkalosis, use of blood products, diuretics, phototherapy, lipid infusions etc
Slide 31-

CLINICAL FEATURES Asymptomatic Symptomatic: a) Neuromuscular irritability,Myoclonic jerks Jitteriness,Exaggerated startle Seizures b)Cardiac involvement:Tachycardia,prolonged QT Interval,decreased contractility, c)Other symptoms like apnea,cyanosis,tachypnea,laryngospasm are noted
Slide 32-

Diagnosis Laboratory: By measuring total or ionised serum calcium Ionised calcium is preferred mode for measuring hypocalcemia ECG: QoTc>0.22 seconds or QTc>0.45 sec QoT is measured from origin of q to origin of t wave QT is measured from origin of q wave to end of t wave
Slide 33-

Management of EOH
Slide 34-

ppt slide no 34 content not found
Slide 35-

Side effects of calcium: Bradycardias Arrythmias Skin and subcutaneous tissue necrosis may occur due to extravasation Hepatic necrosis may occur if tip of uvc lies in branch of portal vein
Slide 36-

LATE ONSET NEONATALHYPOCALCEMIA presents at the end of the first wk of life. It is usually symptomatic in the form of neonatal tetany or seizures. This is usually caused by high phosphate intake (iatrogenic).
Slide 37-

CAUSES OF LATE ONSET HYPOCALCEMIA Increased phosphate load Cow milk, renal insufficiency Hypomagnesemia Vitamin D deficiency Maternal vitamin D deficiency Malabsorption Renal insufficiency Hepatobiliary disease PTH resistence Transient neonatal pseudohypoparathyroidism
Slide 38-

Hypoparathyroidism Primary Hypoplasia, aplasia of parathyroid glands - (Di George’s syndrome), CATCH 22 syndrome ,activating mutations of calcium sensing receptor Secondary Maternal hyperparathyroidism Metabolic Syndromes Kenny-caffey syndrome Long-chain fatty acyl CoA dehydrogenase deficiency Kearns-sayre syndrome
Slide 39-

Iatrogenic Citrated blood products, Lipid infusions, Bicarbonate therapy Diueretics, Glucocorticosteriods Phosphate therapy , Alkalosis Phototherapy
Slide 40-

ppt slide no 40 content not found
Slide 41-

Thank you