Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterized by hyperglycemia, dehydration, and metabolic acidosis. It is diagnosed based on blood sugar over 14 mmol/L, presence of ketones, pH below 7.3, and bicarbonate below 18 mmol/L. Management involves rapid intravenous fluid resuscitation, gradual rehydration and electrolyte replacement, and insulin therapy to reverse hyperglycemia and ketosis while closely monitoring for complications. The goals are to correct estimated fluid deficits over 24 hours and lower blood glucose by 3-4 mmol/L per hour.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
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.
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.
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.
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.
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.
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.
The Many Faces of Hyperparathyroidism & Advances in TreatmentBabak Larian
Hyperparathyroidism is a rare disease that affects the whole body and can cause potentially debilitating symptoms. Unfortunately, parathyroid disease is often poorly understood, even by parathyroid specialists. Because the signs and symptoms of hyperparathryoidism are similar to other conditions (including aging, stress, depression, menopause, fibromyalgia, etc.), patients are often misdiagnosed. As such, it is Dr Larian's goal to educate both physicians and patients more on the different manifestations of the disease and treatment so that patients can receive the care they deserve.
This presentation - The Many Faces of Hyperparathyroidism & Advances in Treatment - has the following objectives:
1- Understand the physiology of parathyroid disease and the molecular basis for it.
2- Be able to identify the different manifestations of hyperparathyroidism: Typical, Normocalcemic Hyperparathyroidism, and Normohormonal Hyperparathyroidism.
3- Understand the reasoning for the latest recommendations for treatment of disease.
For more information about hyperparathyroid disease and surgery please visit www.ParathyroidMD.com or call 310-461-0300.
Clinical Practice Guidelines initiative by the Healthcare Quality Directorate of the Alexandria University Hospitals, Alexandria, Egypt. For further details please refer to http://onlinelibrary.wiley.com/doi/10.1111/jep.12479/full
تم تحميل هذا الملف من
منتديات تمريض مستشفى غزة الاوروبي
http://egh-nsg.forumpalestine.com/
لتحميل اجمل واروع المحاضرات فقط قم بزيارتنا وسوف تكون من الاوائل
مع تحيات المدير العام
علاء شعت
- 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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
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 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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
2. Diabetic ketoacidosis (DKA) is a life
threatening medical emergency
characterised by
1. Hyperglycaemia
2. Dehydration
3. Metabolic acidosis
4. Ketonuria.
3. CRITERIA FOR THE DIAGNOSIS OF DKA
Blood sugar >14.0 mmol/l
Presence of urinary or plasma ketones
ph< 7.3
serum bicarbonate of less than 18 mmol/l.
The main differential diagnosis is the
hyperosmolar hyperglycaemic syndrome which
differs in the extent of dehydration, acidosis and
ketosis.
Patients with hyperosmolar hyperglycaemic
syndrome tend present with a ph>7.3.
4. FREQUENCY AND CAUSES
Diabetic ketoacidosis (DKA) primarily occurs in
patients with Type I diabetes mellitus but it is
being recognised in some Type II diabetics.
The incidence of DKA is estimated at between
4.6 and 8 episodes per 100 patient years of
diabetes.
DKA may be the first presentation of diabetes
or may follow a precipitating event.
The most common precipitant is an infection
however in a large number of cases no
identifiable cause can be found.
5. PRECIPITATING EVENTS OF DKA
Infections (commonly urinary tract) 30%
Non-compliance with treatment 15%
New diagnosis of type I diabetes 5-15%
Other stresses (MI, alcohol, pancreatitis,
drugs) 5%
No cause found in 40%
6. PATHOPHYSIOLOGY
It is due to insulin deficiency, together with an
excess of the counter-regulatory hormones,
glucagon, growth hormone and the
catecholamines.
The absence of insulin results in poor glucose
utilisation by peripheral tissues.
Glucagon, growth hormone and the
catecholamines increase triglyceride breakdown
into free fatty acids and promote glucose
production from hepatic gluconeogenesis.
7. The Ketones, acetoacetate and β
hydroxybutyrate are formed by the beta
oxidation of the free fatty acids.
Hence resulting in hyperglycaemia and the
formation of ketoacids which are the primary
metabolic derangements in DKA.
8. The secondary consequences of these
primary derangements include metabolic
acidosis and an osmotic diuresis.
Metabolic acidosis is caused by the
production of H+ ions by the dissociation of
ketoacids.
The accumulation of ketoacids leads to an
elevated anion gap. This is a key feature of
DKA
9. Initially as the blood sugar rises there is a
shift of fluid from the intracellular to the
extracellular compartment with subsequent
dilution .
Once the blood sugar level exceeds the renal
threshold for glucose, around 12 mmol/l,
glycosuria occurs followed by an obligatory
osmotic diuresis, resulting in a loss of water
from the extracellular compartment.
This hyperglycaemia induced osmotic
diuresis as well as causing a urinary loss of
water and glucose will also cause a loss of,
ketones, sodium, potassium and phosphate
in the urine.
At presentation patients are often severely
dehydrated with marked serum electrolyte
disturbances
10. CLINICAL FEATURES
There is a wide spectrum of severity of illness
in patients presenting with DKA.
Classically patients present with a history of
thirst, polyuria and polydipsia although these
are not invariably present.
Diabetes Mellitus may not have been
previously diagnosed.
Other symptoms may include:
• Weakness and lethargy
• Nausea and vomiting
• Abdominal pain
• Weight loss
11. Common general physical signs are:
• Evidence of dehydration
• Tachycardia and hypotension
• Kussmaul respiration (deep rapid respiration to
provide respiratory compensation for metabolic
acidosis)
• Ketotic breath (fruity acetone smell due to
exhaled ketones)
• Temperature is usually normal or low even in the
presence of an underlying infection.
• Altered consciousness and confusion
12. INVESTIGATIONS
Initial investigations are aimed at confirming the
diagnosis, estimating the severity and identifying
underlying causes.
Blood glucose measured hourly, this will be grossly
elevated at presentation but can rarely be normal if
there has been administration of insulin, resulting in
correction of the blood sugar but not the acidaemia.
When the blood sugar is grossly elevated at
presentation, point of care testing can be inaccurate
and therefore samples should be sent to the
laboratory initially.
13. Urine test for ketones If the nitroprusside
method is used β hydroxybutyrate will not be
measured.
As β hydroxybutyrate is the main ketone
produced in DKA for on-going assessment of
ketonaemia direct measurement of serum β
hydroxybutyrate is recommended but is
dependent on laboratory availability.
14. Serum urea and electrolytes
These should be measured every 2-4 hours
initially.
Sodium
hyperglycaemia will cause a dilutional
hyponatraemia. The measured serum Na can
be corrected by adding 1.6mmol/l for each
5.5mmol/l elevation of serum glucose over
5.5mmmol/l. Correction formula: Corrected Na =
Measured Na + 1.6 [Plasma Glucose (mmol/l) –
5.5/ 5.5]
15. Potassium
In DKA there is a total body deficit of potassium
but because of acidosis and dehydration initial
serum levels may be within the normal range or
be elevated.
Serum levels must be regularly checked
because correction of the acidosis and
administration of insulin can result in a
precipitous drop in serum potassium because of
the intracellular movement of potassium.
16. Urea and creatinine
Renal impairment may be present at
presentation.
Elevated acetoacetate levels may cause a
falsely elevated creatinine level if the
calorimetric method is used to measure the
serum creatinine.
Serum Osmolality Calculated as 2(Na) +
Glucose + Urea.
If a patient in DKA is comatose with an
osmolality less than 330mOsm/kg then other
sources for coma should be sought.
17. Venous or arterial blood gas
This is required every 2-4 hours.
Venous blood gases or venous serum
bicarbonate are an acceptable alternative to
arterial blood gas sampling in the initial
management of DKA as studies have confirmed
that venous blood pH closely reflects arterial
blood pH in these patients.
The venous pH is 0.02-0.03 units lower than
the arterial pH.4
18. Anion gap
An elevated anion gap metabolic acidosis is
a key feature of DKA.
Anion gap is calculated as (Serum Na + K) –
(Serum HCO3 + Cl).
Normal values are 8 – 12mmol/l.
19. Full blood count
An increased white blood cell count in the
range 10-15x 109/ l is characteristic of DKA
and is not indicative of infection.
However a count >25 x 109 should raise
concern that an infection is present.
20. Amylase
Amylase is often raised in the absence of
pancreatitis.
This may cause diagnostic confusion,
especially in the presence of abdominal pain.
Chest X-ray, blood cultures, urine cultures, ECG
and cardiac enzymes should be considered to
investigate potential underlying causes.
Children should be weighed to guide fluid and
drug therapy. If this is not possible an estimated
weight should be calculated.
22. INITIAL ASSESSMENT AND RESUSCITATION
Patients with DKA may be severely unwell and
comatose.
Initial assessment involves confirmation of the
diagnosis and a rapid assessment of Airway,
Breathing ,Circulation and Disability.
Intravenous access is obtained as soon as
possible and blood tests taken for urgent
analysis including blood for culture.
There should be application of 100% oxygen via
a face mask with a reservoir bag.
23. The basic principles of DKA management
1. rapid restoration of adequate circulation and
perfusion with isotonic intravenous fluids
2. gradual rehydration and restoration of
depleted electrolytes
3. insulin to reverse ketosis and
hyperglycaemia
4. careful, regular monitoring of clinical sings
and laboratory tests to detect and treat
complications.
24. FLUIDS
Initially fluid therapy is aimed at rapid
restoration of the intravascular volume.
In the first hour 0.9% saline is given at a rate
of 15-20mls/kg or an average 1-1.5 litres.
Thereafter further fluid therapy should be
administered at a rate sufficient to maintain
adequate blood pressure, urine output and
mental status.
The aim is to correct the estimated water
deficit over 24hours , in general a rate of 4-
14mls/kg/hour will suffice.
25. Patients in cardiogenic shock will require inotropes
and haemodynamic monitoring.
Although some have argued that Hartmann’s solution
is a better fluid to give during the initial resuscitation
as it avoids the hyperchloraemic acidosis.
However adverse sequelae from Hartmann’s include
an increase in the blood glucose from the lactate
load, the potassium it contains (5 mmol/l) can elevate
the serum potassium dangerously in those already
hyperkalaemic and lastly the hypotonicity could
precipitate cerebral oedema.
26. Following the initial period of resuscitation the
subsequent choice of fluid will depend on the
corrected serum sodium.
If normal or elevated then 0.45% saline should be
given, if low then saline should be continued.
When the blood glucose is 14 mmol/l the fluid
should be changed to 5% dextrose with 0.45%
saline until the acidosis and ketosis have resolved.
Slow correction of metabolic abnormalities,
particularly elevated serum sodium and glucose is
a goal of treatment.
Over rapid or excessive fluid therapy in DKA may
precipitate acute cerebral oedema.
27.
28. Insulin
Insulin should be given intravenously and not
subcutaneously.
Once hypokalaemia has been excluded an
intravenous insulin infusion should be
commenced (50 units actrapid in 50 mls 0.9%
saline) at 0.1units/kg/hour.
many protocols advised bolus doses of insulin
at the time of diagnosis of DKA to allow rapid
correction of blood sugar is no longer accepted
practice.
29. Intravenous fluid resuscitation alone will
reduce plasma glucose levels by two
methods. It will dilute the blood glucose
levels and also the levels of counter-
regulatory hormones.
Excessive insulin therapy causes
inappropriately rapid falls in plasma glucose
and risks profound hypokalaemia.
30. A reasonable target for the fall in plasma
glucose is 3-4 mmol/l/hour, if the blood glucose
fails to fall at this rate the insulin rate should be
doubled every hour until the target decrease is
reached.
In those in whom the rate of fall of plasma
glucose exceeds 5 mmol/l/hr the rate should be
reduced to 0.05 units/kg/hr but only for a short
time as a rate of 0.1 units/kg/hr is needed to
switch off ketone production.
31. When the blood glucose falls to below 14 mmol/l a
dextrose containing fluid should be commenced. If
hypoglycaemia occurs prior to complete A
reasonable target for the fall in plasma glucose is
3-4 mmol/l/hour, if the blood glucose fails to fall at
this rate the insulin rate should be doubled every
hour until the target decrease is reached.
In those in whom the rate of fall of plasma glucose
exceeds 5 mmol/l/hr the rate should be reduced to
0.05 units/kg/hr but only for a short time as a rate
of 0.1 units/kg/hr is needed to switch off ketone
production.
When the blood glucose falls to below 14 mmol/l
a dextrose containing fluid should be commenced
If hypoglycaemia occurs prior to complete
32. Potassium replacement In DKA there is a
total body deficit of potassium but despite
this at presentation mild to moderate
hyperkalaemia is not uncommon.
Serum levels will fall once insulin and fluids
are started. Adding 20-40 mmol/l KCl will
usually result in adequate replacement,
keeping the serum potassium around 4.5
mmol/l.
33. If the initial serum potassium is low initially
(<3.3 mmol/l) then the insulin infusion should
be withheld temporarily.
If anuria or peaked ECG T waves are
present at presentation then omit potassium
in the initial fluid replacement until serum
potassium is known. If the serum K is >5.3
mmol/l omit potassium and continue to check
the serum potassium every 2 hours
34. SODIUM BICARBONATE
Sodium bicarbonate is rarely, if ever, necessary.
If administered, deleterious effects include risk
of
hypokalaemia,
cerebral oedema and
reduced tissue oxygenation
by its effects on the oxygen dissociation curve.
Sodium bicarbonate should only be considered
in patients with profound acidosis (pH < 6.9) and
circulatory failure resistant to inotropes.
35. Oral diet should be resumed as soon as the
patient is able.
Subcutaneous insulin regimes may be
commenced when the patient is tolerating an
oral diet and the level of ketonuria has fallen to
1+ or 0.
This usually corresponds to a pH of > 7.3.
Twenty to thirty minutes before a meal
subcutaneous insulin should be given and the
intravenous insulin continued for another 2
hours.
36. ANTIBIOTIC THERAPY
Occult infections are common precipitants of
DKA.
Evidence of infection should be actively sought
and investigations should include blood cultures
and urine dipstick testing and cultures.
Suspected bacterial infections should be treated
aggressively with appropriate antibiotics.
The role for prophylactic antibiotics in patients
with DKA is an area of debate and clinicians
should follow local hospital guidelines.
37. Thromboprophylaxis
Patients with DKA are at increased risk of
thromboembolism.
Prophylactic heparin has an accepted role in the
management of patients with DKA.
It should be continued until the patients are
mobile with no evidence of dehydration or
elevated serum osmolality.
Unfractionated heparin or low molecular weight
heparin are suitable treatments.
38. Nasogastric tube drainage
DKA causes gastric stasis.
Aspiration pneumonitis may occur if
vomiting is combined with a reduced level
of consciousness.
Nasogastric tube drainage should
therefore be considered in all patients with
DKA.
It is mandatory in those with markedly
impaired conscious level.
39. Urinary catheterisation
Strict fluid balance is required in the
management of DKA.
Measurement of urinary output is simplified
by urinary catheterisation.
Continuous ECG monitoring This is indicated
in the presence of significant underlying
cardiac disease, significant hyper- or
hypokalaemia or severe DKA.
40. Notes recording Adequate recording of
regular clinical assessments and laboratory
test results is vital.
This process is made easier by the use of
standard ward or high dependency care
observation charts and serial results sheets
for blood results.
This allows staff to rapidly and accurately
assess patient progress.
42. Although the pathophysiology behind DKA in children
is the same as in adults there are important
differences with respect to presentation and
management.
The young child will be difficult to obtain the classical
history of polyuria, polydipsia and weight loss and as
a consequence may be misdiagnosed initially.
A high proportion of children will present in DKA as
newly diagnosed diabetics and in adolescents the
leading cause of recurrent DKAs is the omission of
insulin.
43. Subtle management differences should be
noted compared with an adult.
Firstly their smaller size mandates a more
precise prescription of fluids and electrolytes.
Secondly cerebral oedema is more common
in children, occurring in up to 1% with a
mortality rate of up to 25%.
44. It is the concern over ensuing cerebral
oedema in children that necessitates a
less aggressive fluid replacement,
avoiding insulin in the first hour of fluid
replacement,
avoiding sodium bicarbonate and
limiting the rate at which the blood glucose falls.
45. RESUSCITATION
Initial management involves confirmation of the
diagnosis and resuscitation of the child using an ABCD
approach (Airway, Breathing, Circulation, and
Disability).
Give 100% oxygen via a face mask with a reservoir
bag and confirm a patent and protected airway.
The child may present comatose, in cerebral oedema,
requiring immediate tracheal intubation.
Establish intravenous access and assess the
circulation (blood pressure, heart rate, pulse volume
and capillary refill time (CRT)).
If the CRT is prolonged or there are other signs of
shock give an initial 10mls/kg of 0.9% saline, followed
by a period of assessment. A further 10mls/kg should
be repeated if the CRT is still prolonged.
46. FLUIDS
Fast and aggressive fluid replacement may increase the
likelihood of cerebral oedema. Fluid replacement is
replaced over 48 hours and is calculated using the
equation:
Fluid requirement over 48 hours = Maintenance (over
48hours) + Deficit- the volume of fluid used in
resuscitation.
Where the deficit (in mls) = Body weight (kg) x %
dehydration x10
And maintenance
= 80 mls/kg/24hours for 3 months -2 years
= 70 mls/kg/24hours for 3-5 years
= 60 mls/kg/24hours for 6-9 years
= 50 mls/kg/24hours for 10-14 years
47. i.e. hourly rate in mls = 48 hour maintenance + deficit (mls) –
resus fluid (mls)
48
The fluid to be given is 0.9% saline with 20
mmols KCl per 500mls unless the patient is
anuric and/or has peaked T waves on the ECG,
in which case the KCl is omitted until the serum
K is known.
During the first hour the blood glucose will fall
rapidly but thereafter a reduction of no more 5
mmols/hour should be permitted.
48. INSULIN
After initiating fluid replacement an hour should
elapse before starting insulin therapy.
As with adults do not use an insulin bolus.
Commence an insulin infusion (50 units actrapid
in 50 mls 0.9% saline) at 0.1units/kg/hour, with
the aim of continuing this rate until the acidosis
has resolved (pH>7.3), extra glucose may
needed to be added to allow for this.
In those in whom the rate of fall of plasma
glucose exceeds 5 mmol/l/hr the rate should be
temporarily reduced to 0.05 units/kg/hr
49.
50. DKA IN PREGNANCY
DKA in pregnancy is of special concern.
It tends to occur at lower plasma glucose levels and
more rapidly than in non-pregnant patients and usually
occurs in the second and third trimesters because of
increasing insulin resistance.
Fetal mortality rates have previously been reported as
high as 30% rising to over 60% in DKA with coma.
However with improvements in diabetic care the
figure for fetal loss has been reported as low as 9% in
some countries.8
Prevention, early recognition and aggressive
management are vitally important to try to minimise
fetal mortality.
It is clear that diabetes and obstetric teams should
jointly manage all pregnant patients with DKA.
52. CEREBRAL OEDEMA
it typically presents within 2 – 24 hours of
treatment for DKA.
Early signs are headache, confusion and
irritability. Later signs include reduced
conscious level and seizures.
The exact pathophysiology is poorly
understood but risk is related to severity and
duration of DKA.
Other suggested associated factors include
overzealous fluid administration, the
administration of sodium bicarbonate and too
rapid fall in the blood glucose.
53. If cerebral oedema is suspected due to an
altered level of consciousness hypoglycaemia
must be excluded initially.
Intravenous mannitol (1.0g/kg = 5.0 ml/kg 20%
mannitol) should be given immediately.
Fluids should be restricted to 2/3 maintenance
and the fluid deficit should be replaced over 72
hours.
Transfer the patient to the Intensive Care Unit
for intubation, mechanical ventilation and
arrangements made for an urgent CT head.
54. HYPOGLYCAEMIA
Hypoglycaemia should be treated with
increased dextrose administration.
A decreased insulin infusion rate may be
necessary temporarily.
Insulin infusions should not be stopped
before the metabolic acidosis and ketonuria
has resolved, as this will delay recovery.
55. HYPOKALAEMIA
Hypokalaemia should be treated in a
standard fashion.
Central venous access will allow potassium
to be safely administered at a rate more than
40 mmol/hr.
Continuous cardiac monitoring is indicated in
this setting.
56. HYPOPHOSPHATAEMIA
Hypophosphataemia is common.
It seldom requires treatment as levels will
correct once oral diet is resumed.
The routine replacement of phosphate does
not improve the outcome in DKA.
However in those with cardiac dysfunction,
anaemia or respiratory depression combined
potassium and phosphate replacement can
be given.
57. SUMMARY
DKA is a potentially life threatening complication of
Diabetes Mellitus.
An understanding of the pathophysiology of the
conditions aids appropriate treatment.
Initial assessment must involve a rapid assessment
of Airway, Breathing and Circulation and obtaining
sufficient intravenous access.
Initial investigations are aimed at confirming the
diagnosis and identifying underlying causes.
The diagnosis of DKA requires a blood sugar >14.0
mmol/l, positive urinary or plasma ketones , an
arterial pH < 7.3 and serum bicarbonate of <
18mmol/l.
58. The basic principles of DKA management
include rapid restoration of adequate circulation
and perfusion with isotonic intravenous fluids,
gradual rehydration and restoration of depleted
electrolytes, insulin to reverse ketosis and
hyperglycaemia and regular monitoring of
clinical signs and laboratory tests to detect and
treat complications.
A target rate of correction of hyperglycaemia is
a drop of blood glucose by 3 – 4 mmol/l/hr.
59. Acute cerebral oedema is a potential
complication possibly due to excessive fluid
therapy or too rapid a fall in blood glucose.
Early signs of the development of this
potentially fatal complication include
headache, irritation and confusion.
Prompt recognition and appropriate
management may improve prognosis.