Transcript DKA farvardin 1395.ppt

IN THE NAME
OF GOD
1
DKA Management
M. Hashemipour
Pediatric Endocrinologist
Isfahan university of medical sciences
Farvardin 1395
2
‫‪Case study‬‬
‫• کودک ‪ 6‬ساله ای با وزن ‪ 20‬کیلو گرم با تنفس تند به‬
‫اورژانس وارد شده‬
‫• در بدو ورود‬
‫• تصمیم شما چیست؟‬
‫‪PH=6.9 ,CO3H= 5‬‬
‫‪NA=135‬‬
‫‪K=5.5‬‬
‫‪BS=624‬‬
‫‪3‬‬
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DKA Defined
• Plasma glucose >200 mg/dl
• Arterial pH <7.30
• Bicarbonate level <15 mEq/l
• ketonemia>3 mmol/L
• Moderate ketonuria
Pediatr Clin N Am 2005
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014
4
parameter
Volume deficit(%)
Co3 H
PH
Blood sugar
BUN
mild
3-5
<15
<7.3
300-400
≥25
moderate
6-10
<10
<7.2
400-600
≥30
severe
10-15
<5
<7.1
>600
>30
Pediatric Diabetes 2014
2006
ISPAD clinical practice consensus guidelines 2014
Endocrinology and Metabolism clinics of north America
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How to Treat DKA
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How to Assess severity of
Dehydration
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Prolonged capillary refill time
Abnormal skin turgor
Abnormal respiratory pattern
sunken eyes, absent tears
weak pulses, and cool extremities
level of consciousness
Pediatric Diabetes 2014
7
Lab Measurement
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Blood gases
Blood or urine ketones
serum electrolytes
Full blood count
Blood urea nitrogen, creatinine
Serum osmolality
ECG for baseline evaluation of potassium
Pediatric Diabetes 2014
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The goals of therapy
 improvement of circulatory volume and
tissue perfusion
 Correct acidosis and reverse ketosis
 slowly Reduction of serum glucose and
plasma osmolarity
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The goals of therapy
 identification and prompt treatment of
comorbid precipitating causes.
 correction of electrolyte imbalance
 Improved glomerular filtration
 increase clearance of glucose and ketones
from the blood
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‫• کودک ‪ 6‬ساله ای با وزن ‪ 20‬کیلو گرم با تنفس تند به‬
‫اورژانس وارد شده‬
‫• در بدو ورود‬
‫‪PH=6.9 ,CO3H= 5‬‬
‫‪NA=135‬‬
‫‪K=5.5‬‬
‫‪BS=624‬‬
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‫‪ ‬چه درجه ای از ‪ DKA‬مطرح است‬
‫‪ ‬درمان را چگونه آغاز می کنید؟‬
‫‪ ‬کنترل قند خون با انسولین چگونه است؟‬
‫‪ ‬قند خون در چه سطحی باید حفظ شود؟‬
‫‪ ‬میزان ونوع مایع دریافتی به بیمار چگونه خواهد بود؟‬
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Severe DKA
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Step1
Fluid Therapy
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Step2
• Evaluation of predisposing factors
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Step3
• Adding K to IV fluid after urination
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Step4
• Insulin therapy
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Step5
Bicarbonate therapy
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Step6
Monitoring
• Vital sign
• Level of consciousness
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Fluid therapy
Maintenance
Deficit
Abnormal ongoing loss
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Fluid deficit
• Grade of dehydration 5% to 10%
• In mild to moderately DKA, fluid deficits 30 to 50
mL/kg.
• In moderate to severe DKA, fluid deficits 50 to
100mL/kg.
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Fluid therapy
1-within first 12 hours
½Deficit +½ Maintenance
2- within next 12 hours
1̸ 4Deficit + ½ Maintenance
• To replace the estimated fluid deficit evenly
Over36- 48 h.
ISPAD clinical practice consensus guidelines 2014
22
‫‪First Method‬‬
‫‪• WT=20kg‬‬
‫‪• Maintenance =1500cc‬‬
‫‪• Deficit =100 *20‬‬
‫‪2000cc‬‬
‫• مایع ‪ 12‬ساعت اول ‪1750=1000+750‬‬
‫• مایع ‪12‬ساعت بعدی ‪1250=750+500‬‬
‫در واقع در ‪ 12‬ساعت دوم و سوم بیمار هر بار‪1250 cc‬‬
‫مایع دریافت می کند‬
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Second Method
• Iv rate= 85cc/kg+maintenance- bolus÷ 23hr
• Iv rate= 85* 20 +1500-300 ÷ 23hr
• Iv rate= 126 cc /hr
Nelson 2014
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Third Method
 First day 1.5-2 times the 24 h maintenance
requirements
 10- 20ml · kg · 1-h
 with isotonic solution 0.9% saline,Ringer’s lactate for
at least 4–6 h
 Then half salin 0.45% salin
 The second day 1-1.5 times the 24 h maintenance
requirements
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
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014
25
Third Method
• WT= 20kg
• Maintenance =1500cc
• Fluid requirement for DKA=2*1500
• Fluid requirement for DKA=1.5*1500
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Pediatric Fluid therapy
Usually 1.5 times the 24 h maintenance
requirements
Urinary losses should not be added to the
calculation of replacement fluids
Pediatrics 2004;113;133-140
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014
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Volume Expansion
• 10-20 ml/kg NS within 60-120 minutes
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Volume Expansion
Repeated 10ml/kg if
1.Shock
2.Hypotension
3.Delay capillary refilling
4.Decrease tissue perfusion
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‫• ساعت ‪ 6‬درمان قند خون بیمار ‪ 250‬است نوع و میزان‬
‫مایع ‪ 6‬ساعت بعدی را بنویسید‬
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Second Method
• Iv rate= 85cc/kg+maintenance- bolus÷ 23hr
• Iv rate= 85* 20 +1500-300 ÷ 23hr
• Iv rate= 126 cc /hr
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‫مایع ‪ 6‬ساعت بعدی‬
‫• ‪126*6 = 756 cc‬‬
‫• دکستروز‪ %5‬همراه با ‪ 75‬میلی اکی واالن درلیتر سدیم‬
‫• در واقع در مایع فوق ‪ 56‬میلی اکی واالن سدیم باید باشد‬
‫• بنابر این در مایع فوق ‪ 18‬سی سی سدیم کلراید ‪ %20‬می ریزیم‬
‫• هر ‪ 1‬سی سی سدیم کلراید ‪ %20‬حاوی ‪ 3.2‬میلی اکی‬
‫واالن سدیم است‬
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Fluid therapy
• Dextrose 5% was added in 0.45%
NS to the rehydrating solution
once the blood glucose fell
to200- 300 mg/dL
Pediatr Crit Care Med 2004
Endocrinol Metab Clin N Am 2006
Pediatric Diabetes 2014
ISPAD clinical practice consensus guidelines 2014
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Fluid therapy
Acidosis with BS 100-200mg/dl
1.Add%7.5 dextrose to solution
2.Insulin should be continue
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Fluid therapy
Acidosis with BS <100mg/dl
1.Add%10 dextrose to solution
2.Insulin should be continue
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Fluid therapy
.
 Administration of intravenous fluids should be
continued until acidosis is corrected and a
patient can tolerate fluids and food.
Pediatr Clin N Am 52 (2005) 1147– 1163
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Fluid therapy
Maintain the blood glucose
100 and 200 mg/dL.
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Fluid therapy
NS with added potassium was used after
urination
Pediatr Crit Care Med 2004 Vol. 5, No. 5
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Potassium
• The plasma potassium concentration should
be rechecked every 1 to 2 hours if the plasma
concentration is outside the normal range.
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Potassium
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K=3-4
40mEq/l
K=4-5
20mEq/l
k<3mEq/l
insulin should be hold temporary
Give 0.5 -1mmol/kg/h iv and oral
Endocrinol Metab Clin N Am 35 (2006) 725–751
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K>5 meq/l
Don’t give K till reversal of k<5meq/l
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Bicarbonate Therapy
After 2-3hours of hydration if
• pH <7.0 or bicarbonate <5 mEq
• Give 1meq/kg over 1 hour
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Indication of Bicarbonate therapy
life-threatening hyperkalemia.
severe acidosis pH<6.9
Hypotension
 shock
Arrhythmia
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Biochemical& Clinical monitoring
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Critical Observations
Hourly blood glucose
Hourly fluid input & output
Neurological status at least hourly
Electrolytes 2 hourly after start of IV therapy
Monitor ECG for T-wave changes
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Biochemical& clinical monitoring
• Repeated 2–4 h, or more frequently, as
clinically indicated
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WARNING SIGNS
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BG falls >90 mg/dL/hour
Headache
Slowing heart rate
Irritability
Decreased conscious level
incontinence
specific neurological signs
Hypoglycemia
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insulin therapy
• Begin with 0.05–0.1 U/kg/h
• 1–2 h after starting fluid replacement therapy
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Insulin therapy
• The administration of insulin without fluid
replacement in such patients with
hypotension may aggrevate hypotension
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‫درمان با انسولين‬
‫• روش اول– مداوم‬
‫ابتدا در ‪ 100cc‬نرمال سالین ‪ 10 ،‬واحد انسولین كریستال مي ریزیم و‬
‫براي بیمار ‪ 0.1iu/kg‬انسولین شروع مي كنیم تا قند خون به ‪300‬‬
‫برسد‪ .‬پس از آن درمان به طریق زیررا بر اساس درجه اسیدوز با یكي‬
‫از دو روش ذیل ادامه مي دهیم‬
‫‪ (a‬اگر اسیدوز باقي باشد دوز انسولین را با نصف ادامه مي دهیم‬
‫‪ (b‬اگر اسیدوز بر طرف شده باشد ‪ ،‬انسولین مداوم قطح مي گردد‪.‬‬
‫نرمال سالین را در میكروست مي ریزیم و هر ‪ 60‬قطره آن ‪cc ،‬‬
‫‪ 1‬است ‪.‬‬
‫حال اگر كودكي ‪ 20‬كیلو باشد و دیابت داشته باشد ‪ ،‬باید درهر ساعت‬
‫‪ 20×0/1=2U‬انسولین بگیرد یعني ‪ 20‬قطره در دقیقه‬
DKA management with SC &IM
insulin
• Initial dose SC: 0.3 unit/kg,
• Followed SC insulin lispro or aspart 0.20
units/kg every 2 h.
 if BG falls to <250 mg/dL before DKA has resolved
Reduce SC insulin lispro or aspart to 0.05
unit/kg per hour
 To keep BG200 mg/dL until resolution ofDKA.
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‫انسولين درماني‬
‫‪-1‬در صورتي که ‪Mild to moderate DKA‬‬
‫انسولین کریستال ‪0.25IU/KG‬هر ‪ 3-4‬ساعت زیر جلدي تزریق مي کنیم‬
Criteria for resolution of DKA
includes
• Glucose <200 mg/dl
• Serum bicarbonate 18 mEq/l
• Venous pH of >7.3.
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Time of feeding
If
• The patient wishes
• Conscious
• No vomiting
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Successful Treatment
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Assess
Reassess
Assess again
Flow sheets
Consider CVP monitoring
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‫• پس از خروج از کتواسیدوزیس چه می کنید ؟‬
‫• ‪0.25iu/kg‬انسولین کریستال هر ‪ 6-4‬ساعت می دهیم‬
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To prevent rebound hyperglycemia
The first SC injection should be given
• 15–30 min with rapid acting insulin
• 1–2 hr with regular insulin
• Before stopping the insulin infusion to allow
sufficient time for the insulin to be absorbed
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Warning signs and symptoms of cerebral edema
 Change in neurological status
 specific neurological signs (cranial nerve
palsies)
 Headache
 Decreased oxygen saturation
 Recurrence of vomiting
 Blood glucose falls > (90 mg//hour
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Warning signs and symptoms of cerebral edema
• Inappropriate slowing of heart rate
• Decrease more than 20 beats/min) not
attributable to improved intravascular volume
or sleep state
• Rising blood pressure>90mmHg
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Risk factors of cerebral edema
• A failure of measured serum sodium levels to
rise or a further decline in serum sodium
levels with therapy is thought to be a
potentially ominous sign of impending
cerebral edema
• Too rapid rise in sodium indicate cerebral
edema result of loss of free water in the urine
from DI
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Risk factors of cerebral edema
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age<5 yr of age
More severe acidosis at presentation
low pCO2
High blood urea nitrogen
New onset diabetes
Bicarbonate treatment for correction of
acidosis
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Risk factors of cerebral edema
• Longer duration of symptoms
• Greater volumes of fluid given in the first 4 h
• Administration of insulin in the first hour of
fluid treatment
• Early fall in glucose-corrected sodium during
therapy
• Greater hypocapnia after adjusting for degree
of acidosis
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Management
• Give mannitol, 0.5–1 g/kg IV over 10–15 min,
and 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
• Restrict IV fluids by one-third
• Move to ICU
• Consider cranial imaging
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• Amount of administered insulin.
• • Hourly (or more frequently as indicated)
accurate
• fluid input(including all oral fluid)and output.
• • Capillary blood glucoseconcentration should
be
• measured hourly
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• 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.
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• The objectives of fluid and electrolyte
replacement
• therapy are:
• • Restoration of circulating volume
• • Replacement of sodium and the ECF and
• intracellular fluid deficit of water
• • Improved glomerular filtration with
enhanced
• clearance of glucose and ketones from the
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• he objectives of fluid and electrolyte
replacement
• therapy are:
• • Restoration of circulating volume
• • Replacement of sodium and the ECF and
• intracellular fluid deficit of water
• • Improved glomerular filtration with
enhanced
• clearance of glucose and ketones from the
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• Satisfactory outcomes have been reported
using
• an alternative simplified method: after an
initial
• fluid bolus of 20 mL/kg of normal saline,
0.675%
• saline (3/4 normal saline, 115.5 mmol sodium)
is
• infused at 2–2.5 times the usual maintenance
rate
70
• ubsequentfluid management (deficit
replacement)
• should be with an isotonic solution (0.9%
saline,
• Ringer’s lactate or Plasmalyte) for at least 4–6
h
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• infuse fluid each day at
• a rate that seldom exceeds 1.5–2 times the
usual
• daily maintenance requirement
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• Start insulin infusion 1–2 h after starting fluid
• replacement therapy; i.e., after the patient
has
• received initial volume expansion
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• (sodium should rise by
• 0.5 mmol/L for each 1 mmol/L decrease in
glucose
• concentration)
74
• If BG falls very rapidly (>5 mmol/L/h) after
initial
• fluid expansion, consider adding glucose even
• before plasma glucose has decreased to 17
mmol/L
• (300 mg/dL).
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• Initial dose SC: 0.3 unit/kg, followed 1 h later
by
• SC insulin lispro or aspart at 0.1 unit/kg every
• hour, or 0.15–0.20 units/kg every 2 h.
• ◦ If BG falls to <14 mmol/L (250 mg/dL) before
• DKA has resolved, reduce SC insulin lispro
• or aspart to 0.05 unit/kg per hour to keep
• BG≈11 mmol/L (200 mg/dL) until resolution of
• DKA.
76
• The starting potassium concentration in the
• infusate should be 40 mmol/L. Subsequent
potassium
• replacement therapy should be based on
serum
• potassium measurements.
• ◦ If potassium is given with the initial rapid
volume
• expansion, a concentration of 20 mmol/L
77
• The maximum recommended rate of IV
potassium
• replacement is usually 0.5 mmol/kg/h.
• • If hypokalemia persists despite a maximum
rate
• of potassium replacement, then the rate of
insulin
• infusion can be reduced
78
hypophosphatemia
• Metabolic encephalopathy (irritability,
paresthesias,
• confusion, seizures, coma); impaired
myocardial
• contractility and respiratory failure due to
• weakness of the diaphragm; muscle
dysfunction
• with proximal myopathy, dysphagia, and
• ileus; rare hematologic effects include
79
• To prevent rebound hyperglycemia, the first
SC
• injection should be given 15–30 min (with
rapidacting
• insulin) or 1–2 h (with regular insulin) before
• stopping the insulin infusion to allow sufficient
time
• for the insulin to be absorbed
80
• degree of edema
• that develops during DKA correlates with the
degree
• of dehydration and hyperventilation at
presentation,CEREBRAL HYPOPERFUSION
• but not with factors related to initial
osmolality or
• osmotic changes during treatment
81
• Disruption
• of the blood–brain-barrier has been found in
cases
• of fatal cerebral edema associated with DKA
(196,
• 197), which further supports the view that
cerebral
• edema is not simply caused by a reduction in
serum
82
increased risk of cerebral edema
include
•
•
•
•
Younger age (198)
• New onset diabetes (170, 198)
• Longer duration of symptoms
or an early fall in glucose-corrected sodium
during
• therapy (83–85, 202).
• • Greater volumes of fluid given in the first 4 h
(88,
• .)202 ,200
83
• Greater hypocapnia at presentation after
adjusting
• for degree of acidosis (85, 183, 200).
• • Increased serum urea nitrogen at
presentation (85,
• .)183
• • More severe acidosis at presentation (88,
201, 202).
• • Bicarbonate treatment for correction of
84
•
•
•
•
•
•
Critical Observations
Hourly blood glucose
Hourly fluid input & output
Neurological status at least hourly
Electrolytes 2 hourly after start of IV therapy
Monitor ECG for T-wave changes
85
• WARNING SIGNS:
• blood glucose falls >5 mmol/l/hour (90 mg/d
L) headache, slowing heart rate,
• irritability, decreased
• conscious level, incontinence,
• specific neurological signs
• Exclude hypoglycaemia
• Is it cerebral edema
86
•
•
•
•
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•
•
•
Management
Give mannitol 0.5-1 g/kg or
hypertonic saline
Restrict IV fluids by one-third
Call senior staff
Move to ICU
Consider cranial imaging
only after patient stabilised
87
•
•
•
•
Abnormal motor or verbal response to pain
• Decorticate or decerebrate posture
• Cranial nerve palsy (especially III, IV, and VI)
• Abnormal neurogenic respiratory pattern
(e.g.,
• grunting, tachypnea, Cheyne–Stokes
respiration,
• apneusis
88
• Major criteria
• • Altered mentation/fluctuating level of
consciousness
• • Sustained heart rate deceleration (decrease
more
• than 20 beats/min) not attributable to
improved
• intravascular volume or sleep state
• • Age-inappropriate incontinence
89
•
•
•
•
•
•
Minor criteria
• Vomiting
• Headache
• Lethargy or not easily arousable
• Diastolic blood pressure >90mmHg
• Age <5 yr
90
• The appearance of diabetes insipidus,
manifested
• by increased urine output with a concomitant
marked
• increase in the serum sodium concentration,
reflecting
• loss of free water in the urine, is a sign of
cerebral
• herniation causing interruption of blood flow
to the
91
•
•
•
•
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 10–15
min, and
• repeat if there is no initial response in 30 min
to 2 h
92
• BARAYE HAR 1 MMOL KAHESH GHAND NA 0.5
MMOL AFZAYESH MIYABAD
93