Fluid therapy in Diabetic ketoacidosis

Dr. Mansoor Elahi

Case report

• A 8 yr old girl first in birth order born out of non- consanguineous parentage brought to casualty with

Chief complaints of Vomitings and Breathlessness associated with fever since 3 days.

Seizure like activity 1 episode & Altered Sensorium since 1 day.

Brief History

• Child was a known diabetic patient and on insulin therapy since 2 years.

• History of discontinuation of insulin for 2 days.

• She didn’t had similar complaints previously.

• On evaluation of history, child was on 15 and 10 units of mixtard insulin in morning and evening respectively.

O/E

• Child was in altered sensorium , her GCS was 6/15

• Sunken eyes

• No pallor / CY / I/ L/ O / CL

• Vitals :

• Temp 100F,

• PR = 146 / min, Low volume pulses, regular rhythm, No radioradial / femoral delay, All peripheral pulses felt

• RR = 58 / min, deep breathing

• BP = 90/50 mmHg, Rt. Arm supine posture

• Saturation was 96% without O2

• Child was put on IV access and sent blood investigations for RBS, VBG analysis.

• Correction of Dehydration :

Started on NS boluses 20ml/kg over 30min, intially with monitoring of vitals and proceeded to further 20 ml/kg as the child was not improving and continued it for 1 hr.

On Monitoring

• Child still in altered sensorium

• Her vitals shows PR = 108/min

• RR = 56/min, Acidotic breathing

• BP = 100/60 mmHg

• Sats were 98% with Oxygen

• Lab reports were as follows RBS = 340 mg/dlNa = 145 meq/lK = 5.3 meq/lCl = 116 meq/lHCO3 = 5 meq/lPH = 7.2, Pco2 = 22 mmHgPO4 = 4 meq/lUrine ketone bodies positive and glucose 3+

Note:

• Correct dehydration first slowly

• Never start insulin bolus

• Never administer bicarbonate until unless indicated.

• Add potassium when K < 5

Most important don’t panic and don’t overcorrect anything.

Monitoring and Investigations:

-Moderate-severe DKA- Admitted in ICU.

-Hrly HR,RR,BP, Spo2, GCS

-Monitor for warning signs of cerebral edema

-2nd hrly monitoring of blood glucose, electrolytes, blood gases, urine ketones were done

-sent blood samples for CBC, Cultures for focus of infection

-X-ray chest to exclude other causes

O/E:

At the time of admission RBS: 330 mg/dl

8:30 am- 312mg/dl

11:30 am- 304mg/dl

PR = 102 bpm

RR = 48 bpm, kussmal breathing

BP = 100/60 mmHg

CNS: altered sensorium GCS = 7/15,

Pupils NSRL, fundus normal,

Tone decreased, tendon reflexes 1+,

Plantars flexors.

CVS: S 1 S 2 +

R/S : B/L NVBS +

P/A: soft , non tender , no organomegaly

DAY 1

Investigations

• Hb = 8.5 g/dl

• TC = 7600 /mm3

• DC = P52, L46, E02

• ESR = 45 mm /1st hr

• Urine ketones + and glucose 2+

• Xray chest was normal

• Blood gases – Na 145 meq/l, K 5.3 meq/l, HCO3

5meq/l, Po4 3.2 meq/l, PH -7.24, Pco2 24mmHg

Treatment plan

• After 1 hour • IV fluids according to Milwaukee formula

80ml/kg + maintenance – bolus23

which gives approx. 90 ml/hr

• Started on Regular Insulin drip @ 0.1 U/kg/hr

• Started on IV Antibiotics, antipyretics

• Don’t administer bicarbornate therapy till ph drops to 7 or cardiac instability occurs.

O/E :

No fresh complaints

Afebrile, hydration adequate

BP: 108/60mmHg, PR: 92bpm, RR : 36/min regular

CNS : GCS – E2 V2 M5 = 9/15

CVS: S 1 S 2 +

R/S : B/L NVBS +

P/A : soft

Day 2

Investigations

• At 5pm, RBS = 320 mg/dl

• PH 7.2, Pco2 26 mmHg, Na 142 meq/l, K 4 meq/l, HCO3 14 meq/l

• RFT were normal, Urine glucose 2+, ketonesweak positive

Invg. continued

• At 9 pm, RBS = 274mg/dl

• Child regains consciousness & her GCS = 13/15

• Started on 5D and ½ NS

• Reduced Insulin drip rate @ 0.05U/kg/hr with Glucose monitoring hrly.

• Treatment started with subcutaneous regular insulin 1U/kg/d

• Should be given 1 hr before stopping insulin drip

Treatment plan

• Child was conscious, alert and well oriented

• Shifted to Gen. ward on day 3.

• Continued IV saline maintenance dose i.e., 1.5L/d

• Started her on mixtard insulin 2/3rd dose before breakfast and 1/3rd before dinner with gradual tapering of regular insulin doses.

• After 6 days, her RBS = 139 mg/dl, urine glucose traces.

• She was now on Mixtard insulin 20 and 10 Units before breakfast and dinner respectively.

Insulin therapy

• Conventional &

• Intensive insulin therapy

- basal dose

- bolus dose

If the metabolic state is not attained correctly, The ‘SEVENTH’S SCALE insulin regime can be started :

Short acting insulin given Q6H with

2/7th total daily dose given before breakfast,

2/7th before Lunch,

2/7th before evening food &

1/7th without food at midnight

Key points to remember

• Correct dehydration first not the glucose• Never administer Bicarbonate unless ph less than

7 associated with/ without cardiac dysfunction.• Fluid deficit should be corrected over 48 hrs

Underhydration is somewhat helpful than overhydration

In our case, altered mental status is bcoz of cerebral acidosis not due to cerebral oedema or electrolyte imbalances

CLASSICAL TRIAD IN DKA

As measurement of ketones in blood is not

readily available, ketonuria is used as a marker

of ketonemia. When measured, serum ketones

(ß hydroxybutyrate plus acetoacetate)

exceed 31 mg/dL with or without ketonuria

>80 mg/dL

Examination

• Fruity odour in breath (ketosis)

• Tachycardia Indicate dehydration or hypovolemia

• Low volume pulses

• Hypotension

• Impaired skin turgor

• Sunken eyes

• Delayed capillary refill time

• Absence of tears

• Weight loss (if premorbid weight known)

• Rapid deep sighing breathing, Kussmaul respiration (metabolic acidosis)

• Changes in sensorium, coma

• Bradycardia, hypertension

• Papilledema Indicate cerebral edema

• Abnormal pupillary reflexes, cranial nerve palsies

• Posturing: decerebrate, decorticate

Investigations

• Leukocytosis with leftward shift is common in DKA due to release of cytokines and catecholamines, and does not necessarily indicate infection

• Cultures (blood and urine) and chest radiograph are obtained if there is suspicion of infection.

• Computed tomography to evaluate for cerebral edema is planned in case examination suggests raised intracranial tension.

TREATMENT OF DKA (Milwaukee DKA PROTOCOL)

Electrolyte disturbances include

Sodium

• Initial serum sodium may be ‘low’ for several reasons:

– Depletion secondary to urinary losses / vomiting

– Hyperlipidemia displaces sodium in the most frequently used laboratory assay, factitiously lowering sodium values.

Hyperglycemia High serum osmolarilty

Water driven from Intra to Extracellular space

Dilutional hyponatremia

• For each 100mg% increase of serum glucose above 100mg%, there is an expected decrease of about 1.6mEq/L in measured sodium.

[Na] + Glucose-100 x 1.6

100

The sodium should increase by about 1.6 mmol/L for each 100mg/dL decline in glucose.

• With prolonged illness & severe DKA, total body losses can approach:

- 10-13 mEq/kg of Sodium

- 5-6 mEq/kg of Potassium

- 4-5 mEq/kg of Phosphate

• Even though Sodium deficit may be repaired within 24 hours, intracellular Potassium & Phosphate may not be completely restored for several days.

Cause of hypokalemia in DKA

• During DKA, intracellular potassium is depleted because of transcellular shifts caused by hypertonicity and in exchange for protons that are buffered intracellularly during metabolic acidosis.

• In turn, this potassium is lost due to hyperglycemia driven osmotic diuresis, and with recurrent vomiting.

• Hyperaldosteronism secondary to volume depletion further exacerbates potassium losses.

• Phosphates are reduced due to tissue catabolism.

• Phosphate correction not needed and their formulas are not available in india

IV Fluids management

• Our goal is to slowly decrease serum glucose

(< 100 mg/dL/hr)

Potassium Administration: General Guidelines

• When initial serum potassium is <2.5 mmol/L (hypokalemia)

Administer 0.5-1 mEq/kg of potassium chloride in IV drip in saline

• Start potassium replacement early, even before starting insulin therapy

• When initial serum potassium is 2.5 - 3.5 mmol/L

Administer potassium 40 mEq/L in IV solution until serum potassium > 3.5 mmol/L

• Monitor serum potassium hourly

• Administer potassium 30 – 40 mEq/L in IV solution to maintain serum potassium at 3.5 –5.0 mmol/L

ECG

HypokalemiaFlattening T wave, wideningof theQT interval, and appearance of U waves

HyperkalemiaTall, peaked symmetrical, T waves and shortening of QT intervals

• When initial serum potassium is 3.5 - 5.0 mmol/L

• Administer potassium 30 – 40 mEq/L in IV solution to maintain serum potassium at

3.5 – 5.0 mmol/L

• Monitor serum potassium hourly

What about bicarbonate administration?

BICARBONATE IS ALMOST NEVER

ADMINISTERED ?– bicarbonate administration leads to increased

cerebral acidosis

• HCO3- combines with H+ and dissociated to CO2 and

H2O. Whereas bicarbonate passes the blood-brain barrier slowly, CO2 diffuses freely, thereby exacerbating cerebral acidosis and cerebral depression

Complications

Cerebral Edema

• Occurs in less than 1% of Pediatric DKA episodes

• Accounts for 60% to 90% of all DKA deaths

• 10% to 25% of survivors have permanent neurological injury

Management of Cerebral Edema

• The head end of the bed should be elevated.

• The fluid administration rate should be reduced by 1/3

• The air way is secured; if warranted by deterioration in sensorium, the patient should be intubated and mechanically ventilated.

• During ventilation, aggressive hyperventilation (PCO2 < 22 mm Hg) should be avoided

• Intravenous mannitol is administered at 0.5–1 g/kg over 20 min; alternatively 3% saline is given as 5–10 ml/kg over 30 min

• The dose is repeated if no response is perceived within 30 min to 2 h.

• Following institution of therapy, a cranial CT is ordered to rule out other treatable causes of neurological deterioration like thrombosis or hemorrhage.

Thank you for your patience