An 18-month old girl presented with diabetic ketoacidosis (DKA). Laboratory tests found a blood glucose of 350 mg/dL, venous pH of 6.9, bicarbonates of 4.8 mmol/L, and ketonuria. The management of DKA involves emergency assessment, supportive care, fluid replacement, insulin therapy, and correction of acidosis, potassium, and phosphate levels. Careful monitoring of clinical signs and laboratory values is important due to risks of cerebral edema, hypokalemia, and other complications.
Hyperg crisittnoon conference hall of coronary circulation of the matters of coronary circulation and my reaction is the matters for men and women with out of India as well as the matters to help someone else and my reaction is the best of the world cup today and today
Hyperg crisittnoon conference hall of coronary circulation of the matters of coronary circulation and my reaction is the matters for men and women with out of India as well as the matters to help someone else and my reaction is the best of the world cup today and today
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
2. An 18-month-old girl presented -
• depressed consciousness, comatose state, pale skin with peripheral cyanosis
• heart rate - 155/min with thread pulse
• respiratory rate - 60/min with Kussmaul breathing
• dry mucous membranes, sunken eyes, poor capillary return, cold fingers and toes
• Weight- 11 kg
• No adenopathy, with normal findings on lung and heart auscultation
Case Vignette
3. • 3 days before admission- the child was agitated, with rare vomiting, elevated temperature,
anorexic and complaining of abdominal pain.
• Her mother consulted a general practitioner, who put her on cotrimoxazole and
paracetamol
• But the child started to vomit ever more frequently and was drowsy.
• The parents took the child to the hospital again, and the doctors tested her for glycemia,
which was 350 mg/dL
6. Concerns in diagnosis
• The younger the child, the more difficult it is to obtain the classical history
• Infants and toddlers in DKA misdiagnosed as having pneumonia, reactive
airways disease (asthma), or bronchiolitis and -treated with glucocorticoids
and/or sympathomimetic agents- exacerbate the metabolic derangements
• duration of symptoms - longer - more severe dehydration and acidosis and
ultimately to obtundation and coma.
7. 15–70% of all newly diagnosed infants and children with diabetes present
with DKA
Risk factors for DKA in newly diagnosed cases -
• younger age (<2 yr)
• delayed diagnosis,
• lower socioeconomic status
• countries with low prevalence of type 1 diabetes mellitus
8. • The risk of DKA in established type 1 diabetes is 1–10% per patient per year
• Risk is increased in -
• Children who omit insulin
• poor metabolic control or previous episodes of DKA.
• Gastroenteritis with persistent vomiting and inability to maintain hydration.
• psychiatric disorders, including those with eating disorders.
• difficult or unstable family circumstances (e.g., parental abuse).
• Peripubertal and adolescent girls.
• Insulin pump therapy (as only rapid- or short-acting insulin is used in pumps,
interruption of insulin delivery for any reason rapidly leads to insulin deficiency)
9. Pathophysiology of Diabetic Ketoacidosis. Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents; a consensus
statement from the American Diabetes Association. Diabetes Care 2006: 29: 1150–1159.
10. Clinical signs and symptoms of DKA –
• Dehydration
• Tachycardia
• Tachypnea (which may be mistaken for pneumonia or asthma)
• Deep, sighing (Kussmaul) respiration; breath has the smell of acetone (described as the
odor of nail polish remover or rotten fruit)
• Nausea, vomiting (mistaken for gastroenteritis)
• Abdominal pain - mimic an acute abdominal condition
• Confusion, drowsiness, loss of consciousness
11. Biochemical criteria
• Hyperglycemia [blood glucose (BG) >11 mmol/L(≈200 mg/dL)]
• Venous Ph <7.3 or bicarbonate <15 mmol/L
• Ketonemia and ketonuria
The severity of DKA is categorized by the degree of acidosis :
• Mild: venous pH<7.3 or bicarbonate <15 mmol/L
• Moderate: pH<7.2, bicarbonate <10 mmol/L
• Severe: pH<7.1, bicarbonate <5 mmol/L.
13. Emergency assessment
• Immediately measure BG and blood BOHB (or urine ketone) concentrations with bedside
meters.
- blood BOHB concentration confirm ketoacidosis (≥3 mmol/L in children) and is
used to monitor the response to treatment
• Perform a clinical evaluation to identify a possible infection
• Weigh the patient
• If body surface area is used for fluid therapy calculations, measure height or length to
determine surface area.
14. • 3 most useful individual signs for predicting 5% dehydration in young children aged 1
month to 5 yr are:
• Prolonged capillary refill time (normal capillary refill is ≤1.5–2 s)
• Abnormal skin turgor (‘tenting’ or inelastic skin)
• Abnormal respiratory pattern (hyperpnea)
• Other useful signs –
- dry mucus membranes,
- sunken eyes, absent tears, weak pulses, and cool extremities.
• ≥10% dehydration - weak or impalpable peripheral pulses, hypotension, and oliguria
Severity of dehydration
19. • Secure the airway and empty the stomach by continuous nasogastric suction to prevent
pulmonary aspiration in the unconscious or severely obtunded patient
• Intubation should be avoided if possible; a sudden increase of pCO2 during or following
intubation may cause cerebrospinal fluid (CSF) pH to decrease and contribute to
worsening of cerebral edema
• Oxygen - patients with severe circulatory impairment or shock.
• Cardiac monitor - electrocardiographic monitoring to assess T waves for evidence of
hyper- or hypokalemia
20. • A second peripheral intravenous (IV) catheter should be placed for convenient and
painless repetitive blood sampling.
• An arterial catheter - some critically ill patients managed in an intensive care unit
• Central venous pressure monitoring - guide fluid management in the critically ill,
obtunded, or neurologically compromised patient
- high risk of thrombosis, especially in the very young
- if a central catheter has been inserted, remove it as soon as the patient’s
clinical status permits
• Insulin should preferably not be given through a central line-
- infusion may be interrupted when other fluids are given through the same line.
21. • Antibiotics- febrile patients after obtaining appropriate cultures of body
fluids.
• Catheterization of the bladder - usually not necessary
- done if the child is unconscious or unable to void on demand (e.g.,
infants and very ill young children)
23. • Deficit in ECF volume - 5–10% .
• Shock - rare in paediatric DKA.
• Clinical estimates of the volume deficit - subjective and inaccurate; either
under- or overestimate the deficit .
• Dehydration - 5–7% in moderate DKA and 10% in severe DKA.
• Effective osmolality - 300- to 350-mosm/l
• Increased serum urea nitrogen and haematocrit - useful markers of the
severity of ECF contraction
• Serum sodium – inaccurate marker ; dilutional hyponatremia and lipemia
Koves IH, Neutze J, Donath S et al. The accuracy of clinical assessment of dehydration during diabetic ketoacidosis in childhood. Diabetes Care 2004: 27:2485–2487
Sottosanti M, Morrison GC, Singh RN et al. Dehydration in children with diabetic ketoacidosis: a prospective study. Arch Dis Child 2012: 97: 96–100
24. Resuscitation fluids
• DKA in shock-
- isotonic saline in 20 mL/kg boluses infused as quickly as possible through a
large bore cannula with reassessment after each bolus.
• Severely volume depleted but not in shock-
- 0.9% saline to restore the peripheral circulation
- 10–20mL/kg over 1–2 h
- may need to be repeated until tissue perfusion is adequate.
• No data to support the use of colloid in preference to crystalloid
25. Replacement fluids
• Isotonic solution (0.9% saline or Ringer’s lactate) for at least 4–6 h
• Deficit replacement after 4–6 h - solution that has a tonicity ≥0.45% saline (0.675%
saline/ 3/4th NS) with added potassium chloride, potassium phosphate or potassium
acetate
• Rate of IV fluid - calculated to rehydrate evenly over at least 48 h
• Infuse fluid each day at a rate - 1.5–2 times the usual daily maintenance requirement
based on age, weight, or body surface area
• Except for severely ill individuals, oral intake typically begins within 24 h
26. Holliday-Segar formula
• 30 kg = 1500 mL + 20 mL* 10 = 1700 mL/ 24 hr (Maintenance fluid requirement )
• Maintenance electrolyte requirements - per 100mL of maintenance IV fluid
27. Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents; a consensus statement from the American Diabetes Association.
Diabetes Care 2006: 29: 1150–1159.
28. Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents; a consensus statement from the American Diabetes Association.
Diabetes Care 2006: 29: 1150–1159.
29. • Clinical assessment of hydration status and calculated effective osmolality - guides to fluid
and electrolyte therapy.
• Aim - gradually to reduce serum effective osmolality to normal
- sodium should rise by 0.5 mmol/L for each 1 mmol/L decrease in glucose
concentration)
• Failure of measured serum sodium levels to rise or a further decline in serum sodium levels
with therapy - potentially ominous sign of impending cerebral edema
• Sodium content of the fluid should be increased - if measured serum sodium concentration is
low and does not rise appropriately as the plasma glucose concentration falls
30. • Large amounts of chloride-rich fluids (combined with preferential renal excretion of
ketones over chloride) - may be associated with hyperchloremic metabolic acidosis
• Chloride load -
- reduced by not giving potassium as potassium chloride
- using fluids such as Ringer’s lactate or Plasmalyte in which a portion of the
chloride is replaced by lactate or acetate, respectively
32. • Rehydration alone frequently causes a marked decrease in BG concentration
• Insulin - normalizes blood glucose and suppreses lipolysis and ketogenesis
• Start insulin infusion 1–2 h after starting fluid replacement therapy; i.e., after the
patient has received initial volume expansion
• Dose: 0.05–0.1 unit/kg/h [e.g., dilute 50 units regular (soluble) insulin in 50mL
normal saline, 1 unit=1mL]
• Route of administration - IV
• An IV bolus should not be used at the start of therapy- may increase the risk of
cerebral edema , can exacerbate hypokalemia and can precipitate shock by
rapidly decreasing osmotic pressure
33. • Dose of insulin -
- 0.05–0.1 unit/kg/h at least until resolution of DKA (pH>7.30, bicarbonate >15
mmol/L, BOHB <1 mmol/L, or closure of the anion gap)
• If the patient shows marked sensitivity to insulin (e.g., some young children with
DKA, patients with HHS, and some older children with established diabetes)-
dose may be decreased provided that metabolic acidosis continues to resolve.
• Insulin has an aldosterone-like effect leading to increased urinary potassium
excretion.
- Time on IV insulin infusion and dose of insulin should be minimized to avoid
severe hypokalemia
34. • During initial volume expansion, the plasma glucose concentration may fall
steeply Thereafter, the plasma glucose concentration typically decreases at a rate
of (54–90 mg/dl/h)
• To prevent an unduly rapid decrease in plasma glucose concentration and
hypoglycemia, 5% glucose should be added to the intravenous fluid when the
plasma glucose falls to 250- 300 mg/dl
• It may be necessary to use 10% or even 12.5% dextrose to prevent
hypoglycaemia while continuing to infuse insulin to correct the metabolic
acidosis
35. Acidosis
• Severe acidosis is reversible by fluid and insulin replacement
• Treatment of hypovolemia improves tissue perfusion and renal function- increasing the
excretion of organic acids
• Insulin stops further ketoacid production and allows ketoacids to be metabolized, which
generates bicarbonate
• Bicarbonate administration may be beneficial in the rare patient with life-threatening
hyperkalemia- 1–2 mmol/kg over 60 min
- may cause paradoxical CNS acidosis and rapid correction of acidosis with
bicarbonate causes hypokalemia
36. Potassium replacement
Deficits of 3–6 mmol/kg ; Causes of deficiency -
• Transcellular shifts of this ion caused by hypertonicity (increased plasma osmolality causes
solvent drag in which water and potassium are drawn out of cells)
• Glycogenolysis and proteolysis secondary to insulin deficiency - potassium efflux from cells
• vomiting
• osmotic diuresis
• Volume depletion causes secondary hyperaldosteronism, which promotes urinary potassium
excretion.
37. • At presentation - serum potassium levels may be normal, increased, or decreased
• Renal dysfunction, by enhancing hyperglycemia and reducing potassium excretion,
contributes to hyperkalemia
• Administration of insulin and the correction of acidosis drives potassium back into the
cells, decreasing serum level
• Potassium replacement therapy is required regardless of the serum potassium
concentration
38. • Hypokalemia- start potassium replacement at the time of initial volume expansion and
before starting insulin therapy
• Otherwise, start replacing potassium after initial volume expansion and concurrent with
starting insulin therapy.
• Hyperkalemia- defer potassium replacement therapy until urine output is documented
• If immediate serum potassium measurements are unavailable- ECG may help to
determine whether the child has hyper- or hypokalemia
• Starting potassium concentration in the infusate - 40 mmol/L
• Continue throughout IV fluid therapy.
• Maximum recommended rate - 0.5 mmol/kg/h.
39. • Potassium phosphate may be used together with potassium chloride or acetate;
e.g.
- 20 mmol/L potassium chloride and 20 mmol/L potassium phosphate
- 20 mmol/L potassium phosphate and 20 mmol/L potassium acetate
• If hypokalemia persists despite a maximum rate of potassium replacement, then
the rate of insulin infusion can be reduced
40. Phosphate
• Deficiency –
- depletion of intracellular phosphate
- osmotic diuresis
- insulin promotes entry of phosphate into cells
- food intake prolonged beyond 24 h
• Prospective studies have not shown clinical benefit from phosphate replacement
• severe hypophosphatemia (1 mg/dl), which may manifest as muscle weakness,
should be treated even in the absence of symptoms
41. • May induce hypocalcemia
- if hypocalcemia develops, administration of phosphate should be stopped
• Potassium phosphate salts may be safely used as an alternative to or combined
with potassium chloride or acetate, provided that careful monitoring of serum
calcium is performed to avoid hypocalcemia
42. Clinical and biochemical monitoring
• flow chart of hour-by-hour clinical observations, IV and oral medications,
fluids, and laboratory results
• Hourly vital signs (heart rate, respiratory rate, blood pressure).
• Hourly neurological observations for warning signs and symptoms of
cerebral edema
• Amount of administered insulin
• Hourly accurate fluid input (including all oral fluid) and output
43. • Capillary blood glucose concentration should be measured hourly
• Laboratory tests: serum electrolytes, glucose, blood urea nitrogen, calcium,
magnesium, phosphorus, hematocrit, and blood gases should be repeated 2–4 h,
or more frequently, as clinically indicated, in more severe cases
• Blood BOHB concentrations every 2 h if available
• Lipids and triglycerides can be grossly elevated causing the blood sample to
show a visible rim of lipids
44. Introduction of oral fluids and transition to SC
Insulin Injections
• Oral fluids - only when substantial clinical improvement has occurred (mild
acidosis/ketosis may still be present)
• IV fluid should be reduced accordingly so that the sum of IV and oral fluids does
not exceed the calculated IV rate (i.e., not in excess of 1.5–2 times maintenance
fluid rate)
• When ketoacidosis has resolved, oral intake is tolerated - change to SC insulin is
planned - the most convenient time to change to SC insulin is just before a
mealtime
45. • To prevent rebound hyperglycemia –
- first SC injection given 15–30 min (with rapid acting insulin)
- or 1–2 h (with regular insulin) before stopping the insulin infusion to allow
sufficient time for the insulin to be absorbed.
• Intermediate / long-acting insulin - overlap should be longer and the rate of IV insulin
infusion gradually lowered.
• Ex - Patients on a basal-bolus insulin regimen, the first dose of basal insulin may be
administered in the evening and the insulin infusion is stopped the next morning.
46. Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents; a consensus statement from the American Diabetes Association.
Diabetes Care 2006: 29: 1150–1159.
47.
48. Algorithm for the management of diabetic ketoacidosis .Adapted from Pinhas-Hamiel and Sperling
51. Morbidity and mortality
• Population studies - mortality rate from DKA in children is 0.15–0.30%
• Cerebral injury - major cause of mortality and morbidity
• Cerebral edema - 60–90% of all DKA deaths
• 10–25% of survivors of cerebral edema have significant residual morbidity
• Children without overt neurological symptoms during DKA treatment may have subtle
evidence of brain injury, particularly memory deficits, after recovery from DKA
53. Cerebral edema
• Incidence of clinically overt cerebral edema - 0.5–0.9%
• Mortality rate - 21–24%
• Mental status abnormalities (GCS scores <14)- 15% of children treated for DKA
• Usually develops - within the first 12 h after treatment has started
- but can occur before treatment has begun or, rarely, may
develop as late as 24–48 h after the start of treatment
54. Risk factors
• Increased serum urea nitrogen at presentation
• More severe acidosis at presentation
• Bicarbonate treatment for correction of acidosis
• Early decrease in serum effective osmolality
• An attenuated rise in serum sodium concentration or an early fall in glucose-corrected
sodium during therapy
• Greater volumes of fluid given in the first 4 h
• Younger age and longer duration of symptoms
55. Pathophysiology
• Fluid influx into the brain caused by rapid declines in serum osmolality and/or overly
vigorous fluid resuscitation
• Recent data suggest that vasogenic, rather than cytotoxic, cerebral edema may be the
predominant finding in DKA
• Activation of ion transporters in the blood-brain barrier may be responsible for fluid
influx into the brain
- result from cerebral hypoperfusion and/or from direct effects of ketosis or
inflammatory cytokines on blood-brain barrier endothelial cells
56. Signs and symptoms
• Headache and slowing of heart rate
• Recurrence of vomiting
• Change in neurological status (restlessness, irritability, increased drowsiness, and
incontinence)
• Specific neurological signs (e.g., cranial nerve palsies, papilledema)
• Rising blood pressure
• Decreased O2 saturation
57. Treatment
• Initiate treatment as soon as the condition is suspected.
• Reduce the rate of fluid administration by one-third.
• Mannitol - 0.5–1 g/kg IV over 10–15 min - repeat if there is no initial response in 30 min
to 2 h
• Hypertonic saline (3%) - 2.5–5 mL/kg over 10–15 min, may be used as an alternative to
mannitol, especially if there is no initial response to mannitol
• Elevate the head of the bed to 30◦.
• Intubation may be necessary for the patient with impending respiratory failure
• Cranial imaging may be considered as with any critically ill patient with encephalopathy
or acute focal neurologic deficit – rule out haemorrhage / thrombosis
58. Prevention of recurrent DKA
• Insulin omission - prevented by comprehensive programs that provide education,
psychosocial evaluation, and treatment combined with adult supervision of the entire
process of insulin administration
• Parents and patients should learn how to recognize and treat ketosis and impending DKA
with additional rapid- or short-acting insulin and oral fluids
• Families should have access to a 24-h telephone helpline for emergency advice and
treatment
59. • Psychosocial reasons for insulin omission :
◦ An attempt to lose weight in an adolescent girl with an eating disorder.
◦ A means of escaping an intolerable or abusive home situation.
◦ Depression or other reason for inability of the patient to manage the diabetes
unassisted
• A psychiatric social worker or clinical psychologist should be consulted to identify the
psychosocial reason(s) contributing to development of DKA