Diabetic Ketoacidosis

Alexandra Wilson MD

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Goals for today

• Understand the pathophysiology of DKA

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• Be confident in managing uncomplicated DKA

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• Be able to manage common issues that arise in patients with DKA

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Type I Diabetes Mellitus: Clinical Manifestations

• Classic presentation of diabetes in children is a history of polyuria, polydipsia, polyphagia, and weight loss.
• Often confused with gastroenteritis in toddlers or acute abdomen in older children.

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DKA : Clinical Manifestation

• Keotacidosis is responsible for the initial presentation of up to 25% of children
• early manifestations are mild and include vomiting, polyuria, and dehydration
• More severe cases include Kussmaul respirations, odor of acetone on the breath
• abdominal pain or rigidity may be present and mimic acute appendicitis or pancreatitis
• cerebral obtundation and coma ultimately ensue

Pathophysiology DKA

Pathophysiology

• Lack of insulin  inability to move glucose into cells. t  breakdown fatty acids and ketogenic proteins to ketoacids to provide energy

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• High counterregulatory hormones(glucagon, cortisol, GH, catecholamines)catabolic state: increased glucose production and decreased utilization

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• When renal threshold of > 180 mg/dL 

osmotic diuresis with urinary losses of electrolytes, dehydration, and compensatory polydipsia

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And how to explain to families

• Insulin is needed to allow cells to bring in glucose
• Without insulin the cells are starving and start breaking down fat and proteins for energy
• This leads to production of acid and high sugar level in the bloodstream
• These make patient feel ill, breath fast and loss fluid and salts

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Many families with child with type 1 DM believe if BG ok it is ok to skip insulin if patient not taking po thus they need to have understanding of BASIC pathophysiology and need for insulin even if BG ok

Risk Factors for DKA

• Initial presentation ( seen in approx 25% cases)
• < 5 years
• Poor access to medical care
• In children with known diabetes
• Risk 1-10/100 person years
• Poor metabolic control/history of DKA
• Psychiatric disorders
• Peripubertal and adolescent girls
• Unstable family situation
• Pump therapy
• The majority of cases are not associated with infection

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Rate and prediction of infection in children with DKA R Flood and V Chiang.�Am J Emerg Med. 2001. 19(4):270-73.

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Classification DKA

• DKA exists when there is hyperglycemia (> 300 mg/dL), ketonemia, acidosis, glucosuria, and ketonuria
• Classified as:
• Mild – pH = 7.2-7.3
• Moderate – pH = 7.1-7.2
• Severe –pH <7.1

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DKA : Treatment

• Treatment is divided into 3 phases
• treatment of ketoacidosis
• transition period
• continuing care and guidance

DKA : Treatment

Goals of treatment of DKA

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• initiation of insulin therapy to correct catabolism, acidosis
• intravascular volume expansion
• correction of deficits in fluids, electrolytes, and acid-base status

DKA : Treatment

• Intravascular volume expansion
• dehydration is most commonly in the order of 10%
• initial hydrating fluid should be isotonic saline
• this alone will often slightly lower the blood glucose
• Treatment of electrolyte abnormalities
• serum K⁺ is often elevated, though total body K⁺ is depleted

DKA: Treatment

• Potassium: K⁺ is started early as resolution of acidosis and the administration of insulin will cause a decrease in serum K⁺
• Phosphate: depleted as well. Phosphate may be added as KPO₄ especially if serum chloride becomes elevated
• Sodium:“Pseudohyponatremia” is often present

Expect that the Na level will rise during treatment

Corrected Na = Measured Na + {(glucose - 100) x 0.016}.

If Na does not rise, be very concerned about SIADH and cerebral edema

DKA Treatment

• Insulin Therapy
• continuous infusion of low-dose insulin IV (~ 0.1 U/kg/hr) is effective, simple, and physiologically sound
• goal is to slowly decrease serum glucose (< 100 mg/dL/hr
• Insulin is used to treat acidosis, not hyperglycemia
• Insulin should rarely be stopped if ongoing acidosis persists

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DKA power plan- phase 1

Initiate this phase ASAP: allows pharmacy to prepare fluids and insulin gtt quickly. If transport for OSH you can call pharmacy with patient age and weight BEFORE they arrive so they can start on prep

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DKA order set- phase 2

All the other important orders are here

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DKA: Traditional approach

• NS IV fluid at 1.5 to 2 x maintenance
• 5% Dextrose is added to IVF when blood glucose is ~ 300 mg/dL
• 10% Dextrose is added when blood glucose is ~ 120 mg/dL

Used sequential types of fluid NS then D% NS then D10 NS to maintain GB in acceptable range as treatment with insulin progressed

2 Bag Method

Allows RN to have fluid readily available and titrate between D10 NS and NS to maintain acceptable BG

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Complications

Cerebral Edema

• Cerebral edema is the major life-threatening complication seen in the treatment of children with DKA
• usually develops several hours after the institution of therapy
• 0.5%-3% of children with DKA will experience catastrophic cerebral edema
• manifestations include headache, ALOC, slurred speech, somnolence VERY late bradycardia, unequal or fixed, dilated pupils
• Increasing evidence suggests that sub clinical cerebral edema occurs in the majority of patients with DKA

Why Does Cerebral Edema Occur?

• Osmotic imbalance between the brain and plasma- due in part to development of “idiogenic osmoles”
• Cerebral hypoxia- dehydration & low Pco2 ↓ blood flow release cytotoxins
• Over-hydration and hyponatremia
• Cerebral acidosis - due to weak organic acids/iatrogenic

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Risk Factors for Cerebral Edema

• Glaser et al 2001 NEJM. 61 children with DKA and cerebral edema c/w 181 random and 174 matched controls.
• Cerebral edema associated with lower Pco2, higher BUN, and treatment with bicarbonate.
• Lawerence et al. 2005 J Peds. Case controlled study . Significant association between CE and inital lower Hco3, higher BUN, higher glucose

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Treatment Cerebral Edema

• Therapy of cerebral edema includes treatment with mannitol and/or 3% saline and modest hyperventilation ( Co2 mid 30s)
• 3% saline - 5cc/kg
• Mannitol 1/2 - 1 gram/kg. Avoid dehydration.
• Rapid sequence intubation (lidocaine, rocuronium + etomidate + fentanyl)

Severe Acidosis

• BICARBONATE IS Rarely ADMINISTERED
• bicarbonate administration may lead 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
• Indicated for cardiovascular compromise
• Consider THAM as alternative

synthetic buffer which does not produce C02

when metabolized Dose – approx. 1 meq/kg

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Hypoglycemia

• Hypoglycemic Reactions (Insulin Shock)
• symptoms and signs include pallor, sweating, apprehension, trembling, tachycardia, hunger, drowsiness, mental confusion, seizures and coma
• management includes administration of IV dextrose or (if conscious) of carbohydrate-containing snack or drink
• glucagon 0.1mg/kg (max 1 mg) is administered to an unconscious or vomiting child without iv access

Transition to sub-Q insulin

• pH > 7.30 and HCO₃ > 17* Be mindful non-anion gap acidosis

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• Patient able to eat
• Subcutaneous insulin:
• Give sq injection, D/C IV insulin / IV dextrose, feed child
• Known diabetes patient
• Usually resume previous dosing
• New patient
• 0.7 – 1.0 units/kg/ day:

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Now some cases…..

Case 1

6 y/o boy is admitted in severe DKA. The family has been traveling and he has been ill for several days.

Initial pH=7.0, K+ = 3.7, glucose is 350mg%.

Despite replacement, his K+ now is 1.9 mg/dl - what do you do?

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A. order 1 meq/kg oral potassium

B order 1 meq/kg IV potassium (max 20 meq)

C. order 1 meq/kg IV potassium and temporarily hold insulin

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Case 1

• Need to treat hypokalemia urgently
• Hold insulin temporarily if K < 2.5*
• Risk Torsades, Vtach, Vfib
• Indication for temporarily holding insulin while tx with KCL

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* attending discretion – some may want it held k< 3.0 especially if delay in getting K supplementation

Case 2

The transport team arrives at the OSH and informs you the potassium on your next admission with DKA is 7.5 on VBG What do you say?

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A. That is normal all patients with DKA are total body K depleted this is an artifact of acidosis

B. Check the patient’s EKG on the bedside monitor

C. Get stat EKG and repeat serum K

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Case 2

• Need EKG with standard lead placement to determine if patient has peaked T waves- bedside monitor may over or under call them
• Repeat stat serum K to confirm but don’t delay treatment if concerns based on EKG

Case 2

You intelligently order an EKG and stat K

What do you do now?

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1. await the stat K result?
2. Give Ca gluconate?
3. Give albuterol and lasix?

Case 2

• Give emergency management hyperkalemia
• Calcium gluconate 30mg/kg FIRST to stabilize myocardium
• Sodium bicarbonate 1meq/kg- to shift K intracellularly
• 1 unit/kg insulin +/- glucose ( as patient is hyperglycemic) – to shift K intracellularly

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B agonist very low efficacy –think about it when was the last time you needed to treat hypokalemia after 1 albuterol neb???

No need kayexalate as patient is not in RF

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Case 3

On arrival to the PICU you note the BG on your new patient with DKA has fallen from 400 to 200 in an hour

pH on most recent BG 7.20

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What action would you take next?

• Stop the insulin drip to prevent further fall in blood glucose
• increase the dextrose content of the IVF
• Increase dextrose content and temporarily decrease insulin infusion rate

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Case 3

• Goal of DKA treatment is to treat acidosis – therefore need insulin
• Try and focus on providing enough glucose to maintain slow decrease in BG (<100mg/dl/hr) and avoid hypoglycemia
• Occasionally need to decrease insulin infusion as well

Case 3

Prior to evening rounds you note the patient is very difficult to arouse

• What concerns do you have ?

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Cerebral edema

Hypoglycemia

Case 3

The patient’s blood glucose is normal but he arouses only to vigorous stimuli and his speech is slurred. Do you

1. get a stat CT scan
2. give 5 cc/kg 3% NS
3. give Nahc03 to treat acidosis and decrease edema

Case 3

• Treat with 3% to increase osmolarity
• CT very poor at diagnosing CE unless severe
• No role for bicarbonate therapy

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Case 4

Your patient is on the usual 1.5 MIVF using

the two-bag method . The insulin gtt is at 0.05 units /kg/hr.

The RN calls during the night and says BG is falling and is now 115. You……..

1. Stop the insulin infusion and transition to SQ insulin since the glucose is now normal
2. Ask for a VBG

Case 4

A VBG will help you determine degree acidosis which allows you to pick best path ( i.e., increase GIR further or wean insulin)

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The pH is 7.22 Hc03 10, what do you do now ?

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1. increase the GIR (dextrose % and/or rate) and temporarily hold insulin
2. Just reduce the insulin infusion

Case 4

• Patient has ongoing ketoacidosis and needs insulin . You should first try to increase the GIR (if needed > 1.5 x maintenance ) and only then decrease insulin to < .05units/kg/hr

Case 5

RN calls you to say patients POC BG is now 40, what do you do ???

1. give 4cc/kg D25 and hold insulin
2. give 2cc/kg D25 and hold insulin
3. decrease insulin gtt to .02 units/kg/hr.

Case 5

• If able to take po – try juice first
• If need IV treatment give 0.5 gram/kg= 2cc/kg D25 or 5cc/kg D10
• Temporarily hold insulin and check VBG to determine degree acidosis to guide ongoing management
• If loss IV access & the patient is difficult to arouse

Glucagon 0.1mg/kg IM (max 1 mg)

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Case 6

15 yo presents to ED with altered MS and the following findings

• serum osm > 320 mOsm
• glucose level > 1000 mg/dL
• Profound dehydration
• pH of 7.3, HCO₃^> 15 mEq/L mild AG acidosis

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Diagnosis ? initial management ??

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Non-Ketotic hyperosmolar hyperglycemia

• Presents in patient with Type 2, and rarely type 1, can present with nonketotic, hyperosmolar, hyperglycemic state
• This is frequently in teens with ready access to quantities of high sugar oral fluids
• Criteria for HNS include serum osmolality of 320 mOsm/kg, plasma glucose level greater than 600 mg/dL (>33.3 mmol/L), profound dehydration, pH of 7.3, HCO₃^- greater than 15 mEq/L, and the absence of severe ketosis.
• Cerebral edema can occur in NKHHS

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NKHHS : Treatment

• Slow correction of hyperosmolar state
• Monitoring and treatment of Cerebral edema
• High Risk for thrombosis

Summary

• DKA: Treat the acidosis, maintain euglycemia

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• DKA: Watch for early signs of cerebral edema

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• Keep a cheat sheet with emergency management of electrolyte abnormalities on your smart phone