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DKA Current Practices in Africa 02 - 02 - 2022-1

This document discusses the current concepts and management of diabetic ketoacidosis (DKA) in children with type 1 diabetes in Africa. It defines DKA and outlines the standard of care, including emergency assessment, supportive measures, clinical and biochemical monitoring, specific insulin therapy, and goals of therapy to correct dehydration, acidosis, ketosis, and blood glucose levels while avoiding complications. The management involves intravenous fluids, insulin therapy, and close monitoring to reverse DKA and improve the patient's condition.

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Raphael Sereti
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0% found this document useful (0 votes)
35 views30 pages

DKA Current Practices in Africa 02 - 02 - 2022-1

This document discusses the current concepts and management of diabetic ketoacidosis (DKA) in children with type 1 diabetes in Africa. It defines DKA and outlines the standard of care, including emergency assessment, supportive measures, clinical and biochemical monitoring, specific insulin therapy, and goals of therapy to correct dehydration, acidosis, ketosis, and blood glucose levels while avoiding complications. The management involves intravenous fluids, insulin therapy, and close monitoring to reverse DKA and improve the patient's condition.

Uploaded by

Raphael Sereti
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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DIABETIC KETOACIDOSIS MANAGEMENT

IN TYPE I DIABETES MELLITUS


Current concepts and practices in Africa

Dr Dipesalema Joel MBBCh, B Med Sc(NUI), MRCPI


Academic Head of Department of Paediatrics and Adolescent Health
Senior Lecturer/Consultant Paediatric Endocrinologist
Faculty of Medicine
University of Botswana
Gaborone
OUTLINE OF THE PRESENTATION

◼ Definitions

◼ Current Concepts in the management of


Diabetes Keto-Acidosis

◼ Current Practices in the management of


Diabetes Keto-Acidosis in children in Africa

◼ Conclusions
Definition of Diabetes Keto Acidosis
◼ A life threatening complication of diabetes characterized by
hyperglycaemia, acidosis and ketosis

◼ Biochemical criteria
❑ Hyperglycemia(blood glucose>11 mmol/l or 200mg/dl)
❑ Venous pH < 7.3
❑ Bicarbonate(HCO3=)<15mmol/l
❑ Ketonaemia or ketonuria

◼ Severity of DKA
❑ Mild-Venous pH<7.3 or HCO3=<15 mmol/l
❑ Moderate-Venous pH<7.2 or HCO3=<10 mmol/l
❑ Severe-Venous pH<7.1 or HCO3=<5 mmol/l
Clinical Manifestation of Diabetes Keto Acidosis

◼ Dehydration

◼ Rapid, deep breathing(Kassmul respiration)

◼ Nausea, vomiting and abdominal pain mimicking acute abdomen

◼ Progressive obtundation and loss of consciousness

◼ Increased leucocytes count with left shift

◼ Non-specific elevation of serum amylase

◼ Fever only when infection is present


Current Standard of Care in the
Management of Diabetes Keto Acidosis
◼ Emergency Assessment
❑ Confirm the diagnosis and determine the cause, carefully look for

evidence of infection.

❑ Weigh the patient

❑ Assess clinical severity of the dehydration

❑ Assess the level of consciousness(AVPU)

❑ Obtain blood samples for laboratory measurement:


◼ serum or plasma glucose, Urea &Electrolytes
◼ venous(or arterial in critically ill patient) pH, pCO2,HCO3=
◼ Ca++, Mg++, PO4=, Plasma Osmolality
◼ HbA1c, Full Blood Count
Emergency Assessment(contd)
◼ Urinalysis for ketones

◼ Beta hydroxybutyrate

◼ Appropriate specimen for culture if there is


infection(Blood, Urine, Throat)

◼ Free insulin levels and C-Peptide

◼ ECG monitoring
Supportive measures
◼ Secure the airways

◼ Place peripheral IV cannula

◼ Use continuous ECG monitoring

◼ O2 for all patients with circulatory impairment

◼ Antibiotics for all febrile patients after cultures


Clinical and Biochemical Monitoring

◼ Use the flow chart to record


❑ Hourly vital signs

❑ Hourly neurological observation

❑ Amount of insulin administered

❑ Hourly fluid input/output

❑ Hourly capillary blood glucose

❑ Blood gas 2 hourly for the 1st 12 hours in severe cases

❑ Labs(U&E, Ca++, Mg++, PO4=, glucose, haematocrit every 4 hours for the first 12 hours in
severe cases.

❑ Urine ketones every 2 hours until cleared

❖ If the laboratory cannot provide timely results, a portable biochemical analyzer that measures plasma glucose,
serum electrolytes and blood ketones on fingerstick blood samples at the bedside is a useful adjunct to laboratory-
based determinations.
Additional Calculations
❑ Anion gap = Na − (Cl + HCO3): normal is 12 ± 2 (mmol/L)

❑ In DKA the anion gap is typically 20–30 mmol/L; an anion


gap >35 mmol/L suggests concomitant lactic acidosis

❑ Corrected sodium = measured Na + 2([plasma glucose


−5.6]/5.6) (mmol/L)

❑ Effective osmolality = (mOsm/kg) 2x(Na + K) + glucose


(mmol/L)
Specific Therapy

◼ Goals of Therapy
❑ Correct dehydration

❑ Correct acidosis and reverse ketosis

❑ Restore blood glucose to normal

❑ Avoid complications of therapy

❑ Identify and treat any precipitating events


PRIYAMBADA ET AL. 1395

Clinical History Biochemical features &


Polyuria, polydipsia Clinical Signs investigations
nocturia, enuresis Dehydration Ketones in urine
Weight loss Deep sighing Increased blood glucose
Nausea, vomiting respiration (Kussmaul) Acidemia (pH <7.3, HCO3
abdominal pain Smell of ketones <15 mmol/L)
Weakness, fatigue Lethargy/drowsiness Urea, electrolytes
Confusion, decreased Other investigations as
level of consciousness needed

Diagnosis confirmed
Diabetic Ketoacidosis
Contact senior staff

Dehydration >5%,
Shock (reduced peripheral pulses) Minimal dehydration
Not in shock
Reduced conscious level/coma Tolerating oral fluids
Acidotic(hyperventilation)
Vomiting

Resuscitation IV Therapy Therapy


Airway ± NG tube Saline 0.9% 10 mL/kg over 1 h; may repeat Start with SC insulin
Breathing (100% oxygen) Calculate fluid requirements Continue oral hydration
Circulation (0.9% saline 10-20 Correct fluid deficit over 36-48 hours†
ml/kg over 1-2 h, repeat until ECG for abnormal T-waves
circulation restored
Add KCl 40 mmol per litre fluid
See Cerebral Edema
management No improvement

Continuous insulin infusion at 0.05-0.1 unit/kg/h


starting 1 hour after fluids initiated

Critical Observations
Hourly blood glucose
Hourly fluid input & output
Neurological status at least hourly
Electrolytes 2 hourly after starting IV fluid therapy
Monitor ECG for T-wave changes Neurological deterioration
WARNING SIGNS:
Severe or progressive
Acidosis not improving headache, slowing heart
Blood glucose ≤17mmol/L (300 mg/dL) rate, irritability, confusion,
or decreased consciousness,
Blood glucose falls 5mmol/L/hour (90 mg/dL) incontinence, specific
Re-evaluate neurologic signs
IV fluid calculations
Insulin delivery system and dose
Need for additional resuscitation IV Therapy
Consider sepsis Change to 0.45% or 0.9% saline; add glucose to Exclude hypoglycemia
fluids (5%-12.5%) to prevent hypoglycemia Is it cerebral edema (CE)?
Adjust sodium infusion to promote an increase
in measured serum sodium
CE management
Give mannitol 0.5-1 g/kg or
3% hypertonic saline
Improved, clinically well, ketoacidosis resolved Adjust IV fluids to maintain
tolerating oral fluids normal BP but avoid over-
hydration
Call senior staff
Move to ICU
Consider cranial imaging
Transition to SC Insulin
only after patient stabilizing
Start SC insulin then stop IV insulin after an appropriate interval

†Fluid deficit to be corrected over 36-48 hours


IV: intravenous; SC: subcutaneous; IM: intramuscular; BG: blood glucose; HCO3: serum bicarbonate

FIG U R E 1 Algorithm for management of DKA as per ISPAD 2018 guidelines1


Current Practices in the Management of Diabetes
Keto Acidosis in Children in Africa

◼ Due to resource limitations, it is not always possible to implement the


current standard of care as outlined in ISPAD guidelines

◼ Among the existing challenges are inadequate nursing staff to provide the
ICU level of care and lack infusion pumps, therefore making it difficult to
give insulin infusion and do close monitoring

◼ Bio-chemical monitoring can be a challenge due to lack of machines to do


blood gas monitoring and UE

◼ There is limited choices of the types of insulin you can use, with insulin

◼ Therefore, the current guidelines have been modified to fit into the resource
limited setting without compromising patient care
KEY POINTS ON OUR CURRENT PRACTICES

◼ Monitoring of clinical and biochemical parameters and


careful replacement of fluid, electrolyte and insulin deficits.

◼ Resuscitation may be required, 1-2 boluses of 10-20 mL/kg


0.9% Saline. Calculate initial fluid rate to give maintenance
fluid volume and correct fluid and electrolyte deficits over
48 hours.

◼ The fluid requirement=maintenance fluid requirement x 1.5

◼ KCl replacement at a rate of 5mmol/kg/day when


resuscitation has been completed. Accomplish this by
adding 20-40 mmol of KCL to a litre of fluid
KEY POINTS ON OUR CURRENT PRACTICES

◼ The starting insulin dose is 0.3 Units/kg of regular short acting human
insulin (Actrapid) stat intramuscularly, followed by a dose of 0.1
Units/kg/hour intramuscularly until acidosis improves HCO3 > 12-
15mmol/L.

◼ Where, the insulin pumps are available, the starting insulin dose is 0.1
Units/kg/hour and this dose should continue to be used until acidosis
improves. Sometimes a higher dose may be required or in special
circumstances this dose may be lower e.g. very young patients or
known sensitivity to insulin.

◼ The aim is to produce a fall in blood glucose of 4 – 5 mmol/L per hour.


Adjustments to the glucose concentration of replacement fluids will be
required if plasma glucose is falling rapidly and/or when glucose
<15mmol/L.
KEY POINTS ON OUR CURRENT PRACTICES

◼ When acidosis has improved, an insulin dose


is adjusted to help maintain plasma glucose
within range 5 – 10mmol/L.

◼ Hypoglycaemia, electrolyte imbalance and


cerebral edema are all potential
complications of therapy that require close
surveillance and management if present
Principles of Water and Salt Replacement

◼ Patients with DKA have a deficit in extracellular fluid (ECF)


volume that usually is in the range 5–10%

◼ Shock with hemodynamic compromise is rare in pediatric DKA

◼ Clinical estimates of the volume deficit are subjective and


inaccurate, therefore, in moderate DKA use 5–7% and in severe
DKA 7–10% dehydration.

◼ Water and salt deficit must be replaced

◼ IV or oral fluids given in another facility should be factored in


deficit and repair
Principles of water and Salt Replacement

• For patients who are severely volume depleted but not in


shock, volume expansion(resuscitation) should begin
immediately with 0.9% saline to restore the peripheral
circulation

• In the rare patient with DKA who present in shock, rapidly


restore circulatory volume with isotonic saline(or Ringer
lactate) in 10-20 mL/kg boluses infused as quickly as
possible through a large bore cannula with re-assessment
after each bolus.

• The volume and rate of administration depends on circulatory


status and where it is clinically indicated, the volume
administered typically is 10 mL/kg/h over 1-2 hours and
maybe repeated if necessary.
Principles of Water and Salt Replacement

◼ Use crystalloid not colloid.There are no data to support the use of


colloid in preference to crystalloid in the treatment of DKA

◼ Subsequent fluid management (deficit replacement) should be with


0.9% saline or Ringer’s acetate for at least 4–6 hours

◼ The rate of fluid (IV and oral) should be calculated to rehydrate evenly
over 48 hours
◼ Requirements=maintenance+deficit
◼ Hourly rate=([maintence for 48 hours+deficit]-all fluid already given)/48
◼ Eg 20 kg 6 years old boy who is 10% dehydrated, has already received 20L/kg saline.
Maintenance; 60 mL X 20 kg=1200 mL in 24 hrs=2400mL in 48 hr
◼ Deficit(mL); 10% X 20kg(≈20000mL)= 2000mL.
◼ Minus 20mL X 20kg=400 mL
◼ Therefore the hourly rate is ([2400+2000]-400mL)/48 =83mL/hr
◼ ALTERNATIVELY, the fluid requirement after initially resuscitation is calculated as Hourly
rate= 1.5 x maintenence rate
Principles of Water and Salt Replacement

◼ In addition to clinical assessment of dehydration, calculation of effective osmolality maybe


valuable to guide fluid and electrolyte therapy
◼ The measured serum sodium concentration is lowered by the dilutional effect of the coexistent
hyperglycemia
◼ Coexistent hyperlipidaemia may also falsely lower the serum sodium measurements, depending
on the method used
◼ An approximate corrected sodium can be calculated as follows
◼ Corrected sodium = measured Na + 2([plasma glucose −5.6]/5.6) (mmol/L)
◼ Effective osmolality = (mOsm/kg) 2x(Na + K) + glucose (mmol/L)
◼ If corrected sodium is greater than 150mmol/L, a hypernatraemic as well as an independent
glucose hyper osmolar state exists and correction of the dehydration and electrolyte imbalance
over 48-72 hours is advocated to minimize the risk of cerebral edema. Consider using 0.45%
normal saline after consultation with an Endocrinologist/Specialist on-call if the corrected Na
continues to rise.
◼ If corrected sodium remains <140mmol/L, continue rehydration with 0.9% saline and slow the rate
of rehydration if the corrected Na continues to fall. Consider 3% saline therapy if signs of raised
intracranial pressure after consultation with an Endocrinologist/Specialist on-call.
◼ Hyponatraemia during treatment usually reflects over-zealous volume correction and insufficient
electrolyte replacement.
◼ NB Large volumes of 0.9% saline are associated with hyperchloremic metabolic acidosis
◼ Urinary losses should not routinely be added to the calculation of replacement fluid, but may be
necessary in rare circumstances
Insulin Therapy
◼ Start insulin infusion 1-2 hours after starting fluid replacement
◼ Correction of insulin deficiency when insulin pumps are NOT
available
❑ Initial dose IM: 0.3 unit/kg, followed 1 hour later by IM short acting
regular insulin(actrapid) at 0.1 unit/kg every hour, or 0.15–0.20 units/kg
every two hours OR

❑ Initial dose SC: 0.3 unit/kg, followed 1 hour later by SC insulin lispro or
aspart at 0.1 unit/kg every hour, or 0.15–0.20 units/kg every two hours

❑ If blood glucose falls to <15 mmol/L (250 mg/dL) before DKA has
resolved, (pH still <7.30), add 5% glucose (e.g., 5% glucose in 0.45%
saline) and continue with insulin as above.

❑ Aim to keep blood glucose at about 11 mmol/L (200 mg/dL) until


resolution of DKA.
Insulin Therapy
◼ Correction of insulin deficiency when insulin pumps are available(Please consult an
Endocrinologist/Specialist on call)
❑ Dose 0.1 units/kg/hour IV (for example, one method is to dilute 50 units regular [soluble] insulin in 50 mL
normal saline, 1 unit = 1 mL)

❑ An IV bolus is unnecessary , may increase the risk of cerebral edema , and should not be used at the start of
therapy

❑ The dose of insulin should usually remain at 0.1 unit/kg/hour at least until resolution of DKA (pH >7.30,
bicarbonate >15 mmol/L and/or closure of the anion gap), which invariably takes longer than normalization of
blood glucose concentrations

❑ If the patient demonstrates marked sensitivity to insulin (e.g., some young children with DKA, patients with
HHS, and some older children with established diabetes), the dose may be decreased to 0.05 unit/kg/hour, or
less, provided that metabolic acidosis continues to resolve.

❑ During initial volume expansion the plasma glucose concentration falls steeply . Thereafter, and after
commencing insulin therapy, the plasma glucose concentration typically decreases at a rate of 2–5
mmol/L/hour, depending on the timing and amount of glucose administration

❑ To prevent an unduly rapid decrease in plasma glucose concentration and hypoglycemia, 5% glucose should
be added to the IV fluid (e.g., 5% glucose in 0.45% saline) when the plasma glucose falls to approximately
14–17 mmol/L (250–300 mg/dL), or sooner if the rate of fall is precipitous

◼ Re-assess if no biochemical improvement


Potassium Replacement
• Replacement therapy is required regardless of serum potassium concentration

◼ If the patient is hypokalemic, start potassium replacement at the time of initial volume
expansion and before starting insulin therapy

• If the patient is hyperkalemic, defer potassium replacement therapy until urine output
is documented

• The starting potassium concentration in the infusate should be achieved by adding


20- 40 mmol of KCL to 1 litre of 0.9% fluid. Subsequent potassium replacement
therapy should be based on serum potassium measurements

◼ Potassium replacement should continue throughout IV fluid therapy


❑ NB Bircarbonate is not recommended for acidosis

◼ The maximum recommended amount of potassium is 40 mmol of KCL per litre of


fluid

◼ If hypokalemia persists despite a maximum rate of potassium replacement, then the


rate of insulin infusion can be reduced.
Complications of Therapy

◼ Inadequate rehydration
◼ Hypoglycaemia

◼ Hypokalaemia

◼ Hypochloremic acidosis

◼ Cerebral edema
Introduction of oral fluids and transition to SC
insulin injections

◼ Oral fluids should be introduced only when


substantial clinical improvement has occurred
(mild acidosis/ketosis may still be present)
◼ When oral fluid is tolerated, IV fluid should be
reduced.
◼ When ketoacidosis has resolved, oral intake is
tolerated, and the change to SC insulin is
planned, the most convenient time to change to
SC insulin is just before a mealtime
Introduction of oral fluids and transition to
SC insulin injections
◼ To prevent rebound hyperglycemia the first SC injection should
be given 15–30 minutes (with rapid acting insulin) or 1–2 hours
(with regular insulin) before stopping the insulin infusion to allow
sufficient time for the insulin to be absorbed. With intermediate-
or long-acting insulin, the overlap should be longer and the IV
insulin gradually lowered. For example, for 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.

◼ The dose and type of SC insulin should be according to local


preferences and circumstances.

◼ After transitioning to SC insulin, frequent blood glucose


monitoring is required to avoid marked hyperglycemia and
hypoglycemia
Cerebral Oedema
◼ In national population studies, the mortality rate from
DKA in children is 0.15% to 0.30%
◼ Cerebral edema accounts for 60% to 90% of all DKA
deaths
◼ The incidence of cerebral edema in national
population studies is 0.5–0.9%
◼ Clinically significant cerebral edema usually
develops 4–12 hours after treatment has started, but
can occur before treatment has begun or, rarely,
may develop as late as 24–48 hours after the start
of treatment
◼ The risk factors of cerebral edema include: younger
age, new onset diabetes and longer duration of
symptoms
Warning Signs and Symptoms of Cerebral
Oedema

◼ Headaches and slowing of heart rate


◼ Change of neurological status(restlessness,
irritability, increased drowsiness,
incontinence)
◼ Specific neurological signs(eg cranial nerve
palsies)
◼ Rising blood pressure
◼ Decreased oxygen saturations
Treatment of Cerebral edema
◼ Initiate treatment as soon as the condition is suspected.
◼ Reduce the rate of fluid administration by one-third.
◼ Give mannitol 0.5–1 g/kg IV over 20 minutes and repeat if there is no
initial response in 30 minutes to2 hours .
◼ Hypertonic saline (3%), 5–10 mL/kg over 30 minutes, may be an
alternative to mannitol or a second line of therapy if there is no initial
response to mannitol.
❑ Mannitol or hypertonic saline should be available at the bedside
◼ Elevate the head of the bed
◼ Intubation may be necessary for the patient with impending respiratory
failure, but aggressive hyperventilation (to a pCO2 <2.9 kPa [22 mm
Hg]) has been associated with poor outcome and is not recommended
◼ After treatment for cerebral edema has been started, a cranial CT scan
should be obtained to rule out other possible intracerebral causes of
neurologic deterioration ( ≈10% of cases), especially thrombosis or
hemorrhage, which may benefit from specific therapy
CONCLUSIONS

◼ Use of intramuscular or subcutaneous insulin


where there are no infusion pumps

◼ Use the dip stick urinalysis to monitor the


ketones where there are no ABG machines

◼ Monitor biochemical parametres 2 hourly


where there is shortage of nursing staff
THANK YOU FOR YOUR
ATTENTION

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