This document discusses diabetic ketoacidosis (DKA) in children. It begins by defining DKA and noting it is the leading cause of morbidity and mortality in children with type 1 diabetes. The pathophysiology of DKA involves insulin deficiency leading to hyperglycemia and ketone production. Diagnosis criteria include hyperglycemia, dehydration, and metabolic acidosis. Management involves correcting dehydration, hyperglycemia, electrolyte imbalances, and the underlying precipitating cause, usually infection. Care must be taken to avoid rapid fluid administration and insulin doses to prevent cerebral edema, a potentially fatal complication of DKA treatment.
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/diabetic-ketoacidosis.html
Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
This is the fifth lecture. it is based on guidelines by NHS UK. the guidelines based are freely available in internet. the source and the used literature are trusted and accurate. i hope this level of a knowledge about the management side of the DKA touches the all areas of patient survival. patho-physiology not discussed here but will be discussed in another lecture in details. to a intern and final year MBBS students or ERPM students must process a level of knowledge described by the lecture. definitely more you read more knowledge you get. get the idea in the lecture and principles of management. so you will be much accurate in a ward. always take superior advice while managing emergencies.
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for energy, which produces ketones. Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose, the body’s normal source of energy. When ketones build up in the blood, they make it more acidic.
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/diabetic-ketoacidosis.html
Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
This is the fifth lecture. it is based on guidelines by NHS UK. the guidelines based are freely available in internet. the source and the used literature are trusted and accurate. i hope this level of a knowledge about the management side of the DKA touches the all areas of patient survival. patho-physiology not discussed here but will be discussed in another lecture in details. to a intern and final year MBBS students or ERPM students must process a level of knowledge described by the lecture. definitely more you read more knowledge you get. get the idea in the lecture and principles of management. so you will be much accurate in a ward. always take superior advice while managing emergencies.
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
Diabetes mellitus (DM) is a common, chronic, metabolic syndrome characterized by hyperglycemia as a cardinal biochemical feature. The major forms of diabetes are classified according to those caused by deficiency of insulin secretion due to pancreatic β-cell damage (type 1 DM, or T1DM) and those that are a consequence of insulin resistance occurring at the level of skeletal muscle, liver, and adipose tissue, with various degrees of β-cell impairment (type 2 DM, or T2DM). T1DM is the most common endocrine-metabolic disorder of childhood and adolescence, with important consequences for physical and emotional development. Individuals with T1DM confront serious lifestyle alterations that include an absolute daily requirement for exogenous insulin, the need to monitor their own glucose level, and the need to pay attention to dietary intake. Morbidity and mortality stem from acute metabolic derangements and from long-term complications (usually in adulthood) that affect small and large vessels resulting in retinopathy, nephropathy, neuropathy, ischemic heart disease, and arterial obstruction with gangrene of the extremities. The acute clinical manifestations are due to hypoinsulinemic hyperglycemic ketoacidosis. Autoimmune mechanisms are factors in the genesis of T1DM; the long-term complications are related to metabolic disturbances (hyperglycemia).
Type 1 Diabetes Mellitus
Formerly called insulin-dependent diabetes mellitus (IDDM) or juvenile diabetes, T1DM is characterized by low or absent levels of endogenously produced insulin and dependence on exogenous insulin to prevent development of ketoacidosis, an acute life-threatening complication of T1DM. The natural history includes 4 distinct stages: (1) preclinical β-cell autoimmunity with progressive defect of insulin secretion, (2) onset of clinical diabetes, (3) transient remission “honeymoon period,” and (4) established diabetes associated with acute and chronic complications and decreased life expectancy. The onset occurs predominantly in childhood, with median age of 7-15 yr, but it may present at any age. The incidence of T1DM has steadily increased in many parts of the world, including Europe and the USA. T1DM is characterized by autoimmune destruction of pancreatic islet β cells. Both genetic susceptibility and environmental factors contribute to the pathogenesis. Susceptibility to T1DM is genetically controlled by alleles of the major histocompatibility complex (MHC) class II genes expressing human leukocyte antigens (HLAs). It is also associated with autoantibodies to islet cell cytoplasm (ICA), insulin (IAA), antibodies to glutamic acid decarboxylase (GADA or GAD65), and ICA512 (IA2). T1DM is associated with other autoimmune diseases such as thyroiditis, celiac disease, multiple sclerosis, and Addison disease. There is some suggestion that high dietary intake of omega-3 polyunsaturated fatty acids and vitamin D supplementation in early childhood decreases the incidence of autoi
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
Diabetes mellitus (DM) is a common, chronic, metabolic syndrome characterized by hyperglycemia as a cardinal biochemical feature. The major forms of diabetes are classified according to those caused by deficiency of insulin secretion due to pancreatic β-cell damage (type 1 DM, or T1DM) and those that are a consequence of insulin resistance occurring at the level of skeletal muscle, liver, and adipose tissue, with various degrees of β-cell impairment (type 2 DM, or T2DM). T1DM is the most common endocrine-metabolic disorder of childhood and adolescence, with important consequences for physical and emotional development. Individuals with T1DM confront serious lifestyle alterations that include an absolute daily requirement for exogenous insulin, the need to monitor their own glucose level, and the need to pay attention to dietary intake. Morbidity and mortality stem from acute metabolic derangements and from long-term complications (usually in adulthood) that affect small and large vessels resulting in retinopathy, nephropathy, neuropathy, ischemic heart disease, and arterial obstruction with gangrene of the extremities. The acute clinical manifestations are due to hypoinsulinemic hyperglycemic ketoacidosis. Autoimmune mechanisms are factors in the genesis of T1DM; the long-term complications are related to metabolic disturbances (hyperglycemia).
Type 1 Diabetes Mellitus
Formerly called insulin-dependent diabetes mellitus (IDDM) or juvenile diabetes, T1DM is characterized by low or absent levels of endogenously produced insulin and dependence on exogenous insulin to prevent development of ketoacidosis, an acute life-threatening complication of T1DM. The natural history includes 4 distinct stages: (1) preclinical β-cell autoimmunity with progressive defect of insulin secretion, (2) onset of clinical diabetes, (3) transient remission “honeymoon period,” and (4) established diabetes associated with acute and chronic complications and decreased life expectancy. The onset occurs predominantly in childhood, with median age of 7-15 yr, but it may present at any age. The incidence of T1DM has steadily increased in many parts of the world, including Europe and the USA. T1DM is characterized by autoimmune destruction of pancreatic islet β cells. Both genetic susceptibility and environmental factors contribute to the pathogenesis. Susceptibility to T1DM is genetically controlled by alleles of the major histocompatibility complex (MHC) class II genes expressing human leukocyte antigens (HLAs). It is also associated with autoantibodies to islet cell cytoplasm (ICA), insulin (IAA), antibodies to glutamic acid decarboxylase (GADA or GAD65), and ICA512 (IA2). T1DM is associated with other autoimmune diseases such as thyroiditis, celiac disease, multiple sclerosis, and Addison disease. There is some suggestion that high dietary intake of omega-3 polyunsaturated fatty acids and vitamin D supplementation in early childhood decreases the incidence of autoi
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
acute complication of diabetes mellitus. cardinal biochemical features for DKA. pathophysiology of DKA. clinical assesment of DKA. investigation and management for DKA. complications of DKA.
Intro to hyperglycemic emergencies - hhs vs dkaPritom Das
Some slides are taken from different textbooks of medicine like Davidson, Kumar and Clark and Oxford, and some from other presentations made by respected tutors. I'm barely responsible for compilation of various resources per my interest. These resources are free for use, and I do not claim any copyright. Hoping knowledge remains free for all, forever.
this power point descripe diabetic ketoacidosis in pediatric age group .. we talk about the risk of it .. management specially (fluid management) as case study .. complications and the treatment of brain oedema .. i hope to be auseful one .. enjoy
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
1. Abdulmoein Eid Al-Agha, MBBS, DCH, CABP,FRCPCH
Professor of Pediatric Endocrinology,
King Abdulaziz UniversityHospital
Website:http://aagha.kau.edu.sa
Diabetes Ketoacidosis
2. 2
Goals & Objectives
• What is DKA?
• Understand the Pathophysiology of DKA.
• Criteria of diagnosis.
• Clinical and laboratory features.
• Discuss the management approach to the patient
with DKA.
• Appreciate the complications that occur during
treatment.
3. • Diabetic ketoacidosis (DKA) is the leading cause of morbidity &
mortality in children with type 1 diabetes mellitus.
• DKA is the major acute complication of type 1 DM.
• DKA can also occur in children with type 2 diabetes
(particularly obese African American adolescents), although at
lower rates than those observed in type 1 diabetes.
• In new-onset diabetes, DKA can be prevented through earlier
recognition and initiation of insulin therapy.
• Caution is necessary in management of paediatric DKA due to
increased risk of cerebral edema, which carries high rates of
morbidity & mortality.
DiabetesKetoacidosis
4. Pathophysiology
• Hyperglycemia as a result of impaired glucose uptake
secondary to insulin deficiency & excess glucagon
secretion.
• Ketone bodies provide alternative usable energy sources in
the absence of intracellular glucose.
• Ketoacids (acetoacetate, β-hydroxybutyrate, acetone) are
products of lipolysis.
• Hyperglycemia causes osmotic diuresis which leads to
excessive loss of free water & electrolytes with secondary
hypovolemia , decreased tissue perfusion & lactic acidosis.
7. Clinical Manifestations
• Ketoacidosis might be, the initial presentation in 25 –
75 % of children with newly diagnosed diabetes.
• Clinical manifestations, in addition to polyuria,
polydipsia & weight loss include:
• Nausea & vomiting.
• Dehydration.
• Kussmaul pattern of breathing.
• Acetone odor on the breath.
• Abdominal pain or rigidity (mimic acute
abdomen).
• Cerebral confusion & coma.
9. Clinical Assessment
• Measure vital signs & assess signs of shock caused by
volume depletion (e.g., decreased blood pressure, reduced
peripheral pulses, tachycardia, & significant postural
changes in blood pressure).
• Measure weight for use in calculating fluid replacement and
insulin infusion rates.
• Estimate the degree of dehydration.
• Assess the neurologic state using the Glasgow Coma Scale
(GCS) or similar assessment initially, then repeated hourly
until the patient is recovered from ketoacidosis and mental
status has returned to normal.
10. Laboratory
• Serum glucose.
• Urinary/plasma ketones.
• Serum electrolytes.
• BUN/Creatinine.
• Serum Osmolality (measured/calculated).
• CBC, blood culture (if infection is suspected).
• Venousblood gas.
• Anion gap : The anion gap can be used as an index of the
severity of the metabolic acidosis
11. 12
Management
Correction of the following:
• Dehydration.
• Hyperglycemia.
• Electrolytes deficits.
• Metabolic acidosis.
• Underlying precipitating factors (Infection,
omission of insulin, stress, ….etc.)
12. Fluid management
• Volume depletion is caused by urinary losses from osmotic
diuresis, as well as gastrointestinal losses from vomiting &
insensible losses from hyperventilation.
• Average water losses in children with DKA are approximately
70 ml/Kg (range 30 - 100 ml/Kg).
• Fluid calculations usually should be based upon degree of
dehydration.
• Children with DKA have a fluid deficit in the range of 5-10%
• Mild DKA 3-5%.
• Moderate DKA 5-7%.
• Severe DKA 10% dehydration.
• Shock is rare in pediatric DKA.
13. Fluid management
• Rapid fluid replacement has been associated with
cerebral edema.
• Initially fluid bolus of 7-10 ml/kg over 60 minutes
(only in severe DKA, otherwise start fluid
rehydration without bolus by maintainace & deficit
replacements
• Fluid deficit should gradually be corrected over 48
hrs.
• Start with NS, then to switch to dextrose 5% with
½ NS, when glucose drop to 250 mg/dl
14. Hyperglycemia Management
• Insulin should be given through intravenous route
& continued till acidosis & dehydration resolved.
• Insulin drips 0.075- 0.1 U/kg/hr (NO BOLUS).
• Gradual correction by reducing serum glucose by 50-
100 mg/dl/hr. (No hurry!).
• Serum glucose often falls after fluid bolus due to increase in
glomerular filtration with increased renal perfusion.
• When acidosis resolved, insulin to be shifted to
subcutaneous route.
• Dextrose should be added to IVF whenever, serum glucose
is less than 250 mg/dl.
• Not lower insulin infusion unless, acidosis has been
resolved.
15. Do not reduce or discontinue the insulin
infusion based solely upon the blood glucose
The insulin infusion should be continued until
Ph >7.30 and/or the HCO3 >15 mmol/l
16. Electrolyte replacements
• Serum sodium & chloride will be corrected gradually
by giving normal saline or 0.45 NS over 48 hours.
• Serum potassium level, is the most important
electrolyte disturbance in patients with diabetic
ketoacidosis.
• A patient with a low serum potassium level should be
assumed to have a potentially life-threatening total
body potassium level.
• As a result of the potential for hypokalemia-induced
dysrhythmias, not to give insulin until potassium
replenishment is underway.
17. Electrolyte replacements
Potassium:
• Initially, might be false normal or high values because of
metabolic acidosis.
• Should be added to fluids as soon as insulin has been started
unless potassium is more than 5.5 mmol/l.
• Be sure of passing urine, prior of giving potassium.
• Total body depletion will become more prominent with
correction of acidosis
• Continuous EKG monitoring is essential.
• Dose of 30-40 mmol/l in either KCl or K phos.
18. Electrolyte replacements
Phosphate:
• Total body depletion will become more prominentwith
correction of acidosis.
• Theoretically, to be corrected but practicallynot
necessarily needed.
• Hypophosphatemia may cause rhabdomyolysis,
hemolysis, impaired oxygen delivery to the tissues.
• Calcium should be monitored during replacement as
acute hypocalcaemia may develop due to intravenous
phosphate infusion.
19. MetabolicAcidosis
• Ketosis & lactic acidosis produce a metabolic acidosis;
however, supplemental bicarbonate is not recommended.
• Acidosis usually resolves with isotonic fluid volume
replenishment and insulin therapy.
• Remember that intravenous insulin & hydration is the
treatment of metabolic acidosis in DKA patients.
• Only indicated in severe metabolic acidosis (pH < 7.0)
or patient is in chock withDKA.
• Studies confirmed that bicarbonate therapy may cause
paradoxical intracellular acidosis, worsening tissue
perfusion, hypokalemia & cerebral edema.
20. 20
MetabolicAcidosis
• Bicarbonate is almost never administered.
• Bicarbonate administration leads to increased
cerebral acidosis.
• Bicarbonate passes the Blood Brain Barrierslowly.
• CO2 diffuses freely exacerbating cerebral acidosis &
depression.
• Indications for bicarbonate use: only in severe acidosis
leading to cardio-respiratory compromise or if PH < 7.
21. Management of underlyingcause
• In each case, we need to look for precipitating factors.
• Infections especially viral is the most common factor.
• Using antibiotics should not be routine in children as most
infections are viral.
• Presence of leukocytosis initially in DKA is due to
dehydration & stress (not usually indicates infection).
• We need to improve education “sick-day managements” in
order to reduce number of DKA episodes.
22. DKA Complications
Cerebral edema
• Occurs in less than 1% of Pediatric DKA episodes.
• Accounts for 60% to 90% of all DKA deaths.
• 10% to 25% of survivors have permanent neurological injury.
• Typically develops within the first 12- 24 hr of treatment.
• Etiology is still unclear.
• Signs & symptoms include:
• Headache.
• Confusion.
• Slurred speech.
• Bradycardia.
• Hypertension.
23. Risk factors for Cerebral edema
• Youngerage (< 5years).
• Severe metabolic acidosis.
• New-onset diabetes.
• Severe dehydration.
• Rapid administration of hypotonic fluids.
• IV bolus of insulin with rapid drop of glucose.
• Usage of bicarbonate.
• Idiopathic (could happen even prior to treatment).
24. Cerebral Edema: Treatment
• Reduce rate of intravenous fluids.
• Elevate head of bed to at least a 30°angle.
• Mannitol 0.25 -1 gram/kg IV over 30 minutes.
• May repeat if no initial response in 30 minutes to 2 hours.
• Intubation for impending respiratory failure but avoid
aggressive hyperventilation.