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Dr Summera Amir
FCPS II
UNIT II
NICH
 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
 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
 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
Height = 134cm below 3rd centile SDS (-1.997)
Weight = 32Kg below 3rd centile SDS (-1.067)
 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
 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
Diabetic ketoacidosis sec to
IDDM
Chronic kideny disease
 CBC :
 Hb : 8.1
 TLC : 10000
 N : 60
 E : 04
 M :03
 L : 40
 Plt : 376000
 Na 152meq/l
 K 5.3meq/l
 Cl 108meq/l
 Serum Calcium 9.3mmol/l
 Serum creatinine 1.1mg/dl
 PH 7.2
 Pco2 20
 Po2 124
 Hco3 10mmol/l
Urinary ketones 150mg/dl
Hb A1c waiting
DKA(diabetic ketoacidosis)
 sec to
IDDM (insulin dependent diabetes
mellitus)
Diabetic ketoacidosis
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%.
 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.
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.
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.
 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.
 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.
 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.
 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.
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.
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.
 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.
Continue the Insulin infusion until acidosis is
cleared:
pH > 7.3.
Bicarbonate > 15 mmol/l
Serum sodium 135-145
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.
 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).
• 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.
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.
 Cerebral Edema
Intracranial thrombosis or infarction.
Acute tubular necrosis.
peripheral edema.
Diabetic ketoacidosis
Diabetic ketoacidosis
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Diabetic ketoacidosis

  • 1.
  • 2. Dr Summera Amir FCPS II UNIT II NICH
  • 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
  • 7. Height = 134cm below 3rd centile SDS (-1.997) Weight = 32Kg below 3rd centile SDS (-1.067)
  • 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
  • 10. Diabetic ketoacidosis sec to IDDM Chronic kideny disease
  • 11.  CBC :  Hb : 8.1  TLC : 10000  N : 60  E : 04  M :03  L : 40  Plt : 376000
  • 12.  Na 152meq/l  K 5.3meq/l  Cl 108meq/l  Serum Calcium 9.3mmol/l  Serum creatinine 1.1mg/dl
  • 13.  PH 7.2  Pco2 20  Po2 124  Hco3 10mmol/l
  • 15. DKA(diabetic ketoacidosis)  sec to IDDM (insulin dependent diabetes mellitus)
  • 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.
  • 35.  Cerebral Edema Intracranial thrombosis or infarction. Acute tubular necrosis. peripheral edema.