Managing DKA at the ER

B. Karuppiah

Consultant – Emergency Department, Kauvery Hospital, Tennur, Trichy

Case presentation

A 48 years aged female was brought in a state of unconsciousness GCS – E2 V2 M4, Pupils – 2.5B/L ERTL

Course in ER – initial assessment 5min TOA

Airway – secretions present

Breathing – RR – 46/min

SpO2 – 68% in room air

Circulation – BP – 100/60mmHg, HR – 145/min

In view of impending respiratory failure and to protect airway, patient was intubated and connected to a ventilator.

History of the patient

Fever15 days on and off, abdominal pain, vomiting, loss of appetite, increased thirst, increased frequency of urine.

Lab Investigations

CBG – 480mg/dl

ABG – pH 7.01

Hco3 – 12

pO2 – 68

Na – 123

K – 3.0

Anionic gap – 18

Urine and Serum ketone – Positive

Diagnostic conclusion in ER 15min TOA

  • DKA with severe metabolic acidosis
  • ? UTI
  • ? SIRS( Systemic Inflammatory Response Syndrome)

Diabetic Ketoacidosis

DKA is a serious acute, life-threatening complication of Diabetes Mellitus. It carries a significant risk of death and morbidity, especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rate of 5–10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before the discovery and use of Insulin (1922), the mortality was 100%.

Epidemiology

DKA is reported in 2–5% of type 1 diabetic patients in industrialized countries, while it occurs in 35–40% of such patients in Africa.

DKA at the time of first diagnosis of diabetes mellitus is reported in only 2–3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries.

Pathophysiology

Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water and sodium loss.

In the absence of insulin activity, the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis.

The excess of ketone bodies will cause metabolic acidosis, the latter is also aggravated by Lactic aAcidosis caused by dehydration and poor tissue perfusion.

Vomiting due to ileus, plus increased insensible water losses due to tachypnea, will worsen the state of dehydration. Electrolyte abnormalities are secondary to their loss in urine and trans-membrane alterations following acidosis and osmotic diuresis

Because of acidosis, K ions enter the circulation leading to hyperkalemia, this is aggravated by dehydration and renal failure. So, depending on the duration of DKA, serum potassium (K) at diagnosis may be high, normal or low, but the intracellular K stores are always depleted.

Phosphate depletion will also take place due to metabolic acidosis. Na+ loss occurs secondary to the hyperosmotic state. The dehydration can lead to decreased kidney perfusion and acute renal failure.

Accumulation of ketone bodies contributes to the abdominal pain and vomiting. The increasing acidosis leads to acidotic breathing and acetone smell in the breath and eventually causes impaired consciousness and coma.

Precipitating Factors

  • New onset of type 1 DM – 25%
  • Infections (the most common cause): 40%
  • Drugs: e.g. Steroids, Thiazides, Dobutamine and Terbutaline.
  • Omission of Insulin – 20%. due to;
  • Non-availability (poor countries)
  • Fear of hypoglycemia
  • Fear of weight gain
  • Stress of chronic disease.

Diagnosis

Should always suspect DKA if a diabetic patient presents with;

  • Acidotic (Kussmaul’s) breathing, with a fruity smell (acetone).
  • Abdominal pain or distension.
  • Any altered mental status ranging from disorientation to coma.

To diagnose DKA, the following criteria must be fulfilled;

  • Hyperglycemia: of > 300 mg/dl & glucosuria
  • Ketonemia and ketonuria
  • Metabolic acidosis: pH < 7.25, serum bicarbonate < 15 mmol/l. Anion gap >10.
  • Anion gap= [Na]+[K] [Cl] –[HCO3] +.

This is usually accompanied with severe dehydration and electrolyte imbalance.

Assessment

History

Symptoms of hyperglycemia, precipitating factors, diet and insulin dose.

Examination

Look for signs of dehydration, acidosis, and electrolyte imbalance, including shock, hypotension, acidotic breathing, CNS status etc.

Look for signs of hidden infections (Fever strongly suggests infection).

Quick Diagnosis

Diabetic Ketoacidosis (DKA)

D – Hyperglycemia, K – Ketonuria and A – Acidosis.

Both Hyperglycemia (using glucometer) glycosuria and ketonuria (with strips) must be done in the ER and treatment started, without waiting for Lab results which may be delayed.

Baseline Investigations

The initial Lab evaluation includes;

  • Plasma and urine levels of glucose & ketones.
  • ABG, U&E (including Na, K, Ca, Mg, Cl, PO4, HCO3) and arterial pH (with calculated anion gap).
  • Venous pH is as accurate as arterial (an error of 0.025 less than arterial pH). Complete Blood Count, RFT and LFT.
  • Further tests e.g., cultures, X-rays, are done when needed.

Pitfalls in DKA

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: Often raised, & when there is abdominal pain, a diagnosis of pancreatitis may be made mistakenly; elevation  in Serum Lipase is more diagnostic

Management

The management steps of DKA include;

  • Assessment of causes and sequel of DKA by taking a short history & performing a scan examination.
  • Quick diagnosis of DKA at the ER.
  • Baseline investigations.
  • Treatment, Monitoring and avoiding complications.
  • Transition to outpatient management.

Treatment

  • Careful replacement of fluid deficits.
  • Correction of acidosis and hyperglycemia via Insulin administration.
  • Correction of electrolytes imbalance.
  • Treatment of underlying cause.
  • Monitoring for complications of treatment.
  • Manage DKA in the ICU.

Insulin Therapy

Continue the Insulin infusion until acidosis is cleared

  • pH > 7.3.
  • Bicarbonate > 15 mmol/l
  • Normal anion gap 10-12.

Correction of Acidosis

Insulin therapy stops lipolysis and promotes the metabolism of ketone bodies. This together with correction of dehydration normalize the blood PH. Bicarbonate therapy should not be used unless severe acidosis (pH<7.0) results in hemodynamic instability. If it must be given, it must infused slowly over several hours.

As acidosis is corrected, urine KB appears to rise. Urine KB are not a prognostic value in DKA

Insulin Therapy

If no adequate settings (i.e. no infusion or syringe pumps and 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 use SC insulin in a dose of 0.25 U/kg every 4 hr.

When a patient is out of DKA return to the previous insulin dose.

Correction of Electrolyte Imbalance

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 is given as KCL and the rest as potassium phosphate, this will provide phosphate for replacement and avoids excess phosphate (may precipitate hypocalcemia) and excess Cl (may precipitate cerebral edema or adds to acidosis).

Monitoring Parameters

  • A flow chart must be used to monitor fluid balance and Lab measures.
  • Serum glucose must be measured hourly.
  • Electrolytes also 2–3 hourly.
  • The Ca, Mg and phosphate must be measured initially at least once during therapy.
  • Neurological and mental state must be examined frequently if any complaints of headache or deterioration of mental status should prompt rapid evaluation for possible cerebral edema.

Complications

  • Cerebral Edema
  • Intracranial thrombosis or Myocardial infarction.
  • Acute tubular necrosis

Cerebral Edema

Clinically apparent cerebral edema occurs in 1-2% of children with DKA. It is a serious complication with a mortality of > 70%. Only 15% recover without permanent damage. Typically, it takes place 6-10 hr after initiation of treatment, often following a period of clinical improvement.

Causes of Cerebral Edema

The mechanism of CE is not fully understood, but many factors have been implicated;

  • Rapid or sharp decline in serum osmolality with treatment.
  • High initial corrected serum Na concentration.
  • High initial serum glucose concentration.
  • Longer duration of symptoms before initiation of treatment.
  • Younger age.
  • Failure of serum Na to raise as serum glucose falls during treatment.

Presentations of Cerebral Edema

  • Deterioration of level of consciousness.
  • Lethargy and decrease in arousal status.
  • Headache and pupillary changes.
  • Seizures and incontinence.
  • Bradycardia and respiratory arrest when brain stem herniation takes place.

Treatment of Cerebral Edema

  • Reduce IV fluids
  • Raise the foot end of the Bed
  • IV Mannitol
  • Elective Mechanical Ventilation
  • Dialysis if associated with fluid overload or renal failure.
  • Use of IV dexamethasone is not recommended.

Key points to take home

  • Start intravenous fluids before insulin therapy
  • Potassium level should be >3.3mEq/L before initiation of insulin therapy ( supplement K if needed)
  • Administer insulin bolus at 0.1U/kg/hr. Measure CBG every hour to adjust the insulin infusion rate.
  • Avoid hypoglycemia during the insulin infusion by initiating dextrose-containing fluids until DKA is resolved
  • Transition to S/C insulin only when DKA is resolved.


Dr. B. Karuppiah
Consultant – Emergency Department

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