A 12-year-old male presented with fever for 15 days, abdominal pain for 1 week, and shortness of breath for 1 day. Examination found the patient to be sick-looking and irritable with mild anemia. Lab results showed metabolic acidosis, ketonemia, and hyperglycemia. The patient was diagnosed with diabetic ketoacidosis secondary to insulin-dependent diabetes mellitus. Treatment involved fluid resuscitation, insulin therapy, electrolyte replacement, and monitoring for complications.
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Diabetic Ketoacidosis, diabetus type 1 complection. diagnosisi and managment
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
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
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
Diabetic ketoacidosis meaning,types &management for nurses murugeshMURUGESHHJ
its an brief information about the Diabetic ketoacidosis, causes, signs & symptoms ,hospital management protocals in simple english......provides more information with diagrammatic way ...thank you all
Diabetic ketoacidosis meaning,types &management for nurses murugeshMURUGESHHJ
its an brief information about the Diabetic ketoacidosis, causes, signs & symptoms ,hospital management protocals in simple english......provides more information with diagrammatic way ...thank you all
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.
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.
Academic discussion/ Lecture class for 5th year MBBS students on Diabetic Emergencies, types, their sign-symptoms and managements. Most of the Data was taken from Davidson's Principles and Practice of Medicine.
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
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3. 12 years old male Ayaz weighing 32 kg resident of
Thatta presented in E.R with complain of
Fever 15 days
abdominal pain 1 week
Shortness of breath 1 day
4.
5. Past History : Unremarkable
Birth history :SVD at home no History of birth
asphyxia or jaundice
Vaccination : only polio drops taken
Developmental Hx : Development appropriate to age
achieved all mile stone acc to age
Nutirional history : satisfactory
Family Hx : 1st issue of consangious marriage
2sister and one brother All are
alright and healthy
Socio-Economic Hx : belong to poor class
family father is labourar
6. Sick looking irritable child
having
VITALS:
H/R : 98b/m
R/R : 48b/m
Temp :A/ f
B.P 105/70mm 50th
centile
My patient is mildly
anemic while there is no
evidence of jaundice
clubbing cyanosis
There is no
lymphadenopathy
8. Systemic examination
RESPIRATORY
Chest :normal vesicular breathing with no added
sounds.
CVS :
S1 + S2 Audible
No added sound present
Abdominal Examination
Abdomen soft non tender . distended no visible vein
No viseromegaly
9. CNS Examination :
irritable child with
Tone .Normal in All limbs
Power : 5/5 in four limbs
Reflex's : normal in all four
Planter: down going
Cranial nerve. Intact
Back examination: normal
Sensory system :intact
17. DKA is a serious acute complications of
Diabetes Mellitus. It carries significant risk of
death and/or morbidity especially with
delayed treatment.
The prognosis of DKA is worse in the extremes
of age, with a mortality rates of 5-10%.
With the new advances of therapy, DKA
mortality decreases to > 2%. Before discovery
and use of Insulin (1922) the mortality was
100%.
18. You should suspect DKA if a
diabetic patient presents with:
Dehydration.
Acidotic (Kussmaul’s) breathing, with a fruity
smell (acetone).
Abdominal pain &or distension.
Vomiting.
An altered mental status ranging from
disorientation to coma.
19. To diagnose DKA, the following
criteria must be
fulfilled :
1. Hyperglycemia: of > 250 mg/dl & glucosuria
2. Ketonemia and ketonuria
3. Metabolic acidosis: pH < 7.25, serum
bicarbonate < 15 mmol/l
This is usually accompanied with severe
dehydration and electrolyte imbalance.
20. The management steps of DKA includes:
Assessment of causes & sequele of DKA by taking a
short history & performing a scan examination.
Quick diagnosis of DKA at the ER.
Baseline investigations.
Treatment, Monitoring & avoiding complications.
Transition to outpatient management.
21. History:
Symptoms of hyperglycemia, precipitating
factors ,
diet and insulin dose.
Examination:
Look for signs of dehydration, acidosis, and
electrolytes imbalance, including shock,
hypotension, acidotic breathing, CNS
status…etc.
Look for signs of hidden infections (Fever
strongly suggests infection) and If possible,
obtain
accurate weight before starting treatment.
22. The initial Lab evaluation includes:
Plasma & urine levels of glucose & ketones.
ABG, U&E (including Na, K, Ca, Mg, Cl, PO4,
HCO3), & arterial pH
Venous pH is as accurate as arterial (an error
of 0.025 less than arterial pH)
Complete Blood Count with differential.
Further tests e.g., cultures, X-rays…etc , are
done when needed.
23. High WCC: may be seen in the absence of
infections.
BUN: may be elevated with prerenal azotemia
secondary to dehydration.
Creatinine: some assays may cross-react with
ketone bodies, so it may not reflect true renal
function.
Serum Amylase: is often raised, & when there
is abdominal pain, a diagnosis of pancreatitis
may mistakenly be made.
24. Principles of Treatment:
Careful replacement of fluid deficits.
Correction of acidosis & hyperglycemia via
Insulin administration.
Correction of electrolytes imbalance.
Treatment of underlying cause.
Monitoring for complications of treatment.
Manage DKA in the PICU. If not available it
can be managed in the special care room of
the pediatric inpatient ward.
25.
26.
27. Determine hydration status:
Hypovolemic shock:
administer 0.9% saline, Ringer’s lactate or a
plasma
expander as a bolus dose of 20-30 ml/kg. This
can
be repeated if the state of shock persists. Once
the
patient is out of shock, you go to the 2nd step of
management.
28. B- Dehydration without shock:
Administer 0.9% Saline 10 ml/kg/hour
for an initial hour, to restore blood
volume and renal perfusion.
The remaining deficit should be added
to the maintenance, & the total being
replaced over 36-48 hours. To avoid rapid
shifts in serum osmolality 0.9% Saline
can be used for the initial 4-6 hours,
followed by 0.45% saline.
29. When serum glucose reaches 250mg/dl
change fluid to 5% dextrose with 0.45
saline, at a rate that allow complete
restoration in 48 hours, & to maintain
glucose at 150-250mg/dl.
Pediatric saline 0.18% Na Cl should not
be used even in young children.
30. Continue the Insulin infusion until acidosis is
cleared:
pH > 7.3.
Bicarbonate > 15 mmol/l
Serum sodium 135-145
31. If no adequate settings (i.e. no infusion
or syringe pumps & no ICU care which is
the usual situation in many developing
countries) Give regular Insulin 0.1
U/kg/hour IM till acidosis disappears
and blood glucose drops to <250 mg/dl,
then us SC insulin in a dose of 0.25 U/kg
every 4 hours.
When patient is out of DKA return to
the previous insulin dose.
32. Regardless of K conc. at presentation, total
body K is low. So, as soon as the urine output is
restored, potassium supplementation must be
added to IV fluid at a conc. of 20-40 mmol/l,
where 50% of it given as KCl, & the rest as
potassium phosphate, this will provide
phosphate for replacement, & avoids excess
phosphate (may precipitate hypocalcaemia) &
excess Cl (may precipitate cerebral edema or
adds to acidosis).
33. • If K conc. < 2.5, administer 1mmol/kg of
• KCl in IV saline over 1 hour. Withhold
• Insulin until K conc. becomes> 2.5 and
• monitor K conc. hourly.
• If serum potassium is 6 or more, do not give potassium
till you check renal function and patients passes
adequate urine.
34. A flow chart must be used to monitor fluid
balance & Lab measures.
serum glucose must be measured hourly.
electrolytes also 2-3 hourly.
Ca, Mg, & phosphate must be measured
initially & at least once during therapy.
Neurological & mental state must examined
frequently, & any complaints of headache or
deterioration of mental status should prompt
rapid evaluation for possible cerebral edema.