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Diabetic Ketoacidosis

- Introduction

➡️Diagnosis of Diabetic Ketoacidosis (DKA): (ISPAD 2022)

▪️ Clinical manifestations of DKA:

o   Dehydration

o   Tachypnea, rapid deep, sighing (Kussmaul’s) respiration

o   Nausea, vomiting without diarrhea, and abdominal pain that may mimic an acute abdominal condition

o   Confusion, drowsiness

Not all children or caregivers give history of classic symptoms of diabetes (polyuria, polydipsia) at the time of diagnosis of DKA, and other symptoms are non-specific (eg, weight loss, fatigue, vomiting, abdominal pain). Therefore, fingerstick blood glucose measurements should be considered for all children presenting with rapid breathing or with vomiting and abdominal pain without diarrhea.

▪️ The biochemical criteria for the diagnosis of DKA are:

o   Hyperglycemia : blood glucose ≈200 mg/dl

o   Venous pH < 7.3 or serum bicarbonate < 18 mmol/L (C)

o   Ketonemia (blood ß-hydroxybuyrate ≥3 mmol/L if available, a sensitive indicator of DKA) (C) or Moderate or large ketonuria. Urinary ketones must be read 15 seconds after stick is dipped.

▪️  The Severity of DKA is categorized by the degree of acidosis: (ISPAD 2022)

o   Mild: venous pH < 7.3 or serum bicarbonate <18 mmol/L

o   Moderate: pH < 7.2 or serum bicarbonate <10 mmol/L

o   Severe: pH < 7.1 or serum bicarbonate <5 mmol/L

▪️Hyperglycemic Hyperosmolar State (HHS): (ISPAD , 2022)

  • Plasma glucose concentration above 600 mg/dl
  • Venous pH > 7.25; arterial pH > 7.30 (arterial sample is not necessary)
  • Serum bicarbonate >15 mmol/L
  • Small ketonuria, absent to mild ketonemia
  • Effective serum osmolality >320 mOsm/kg
  • Obtundation, combativeness, or seizures (in approximately 50%)

Formerly called Hyperosmolar non-ketotic coma, it is characterized by extremely elevated serum glucose concentrations and hyperosmolality without significant ketosis or acidosis. HHS manifests with gradually increasing polyuria and polydipsia that may go unrecognized resulting in profound dehydration and electrolyte losses at the time of presentation. HHS may occur in children with type 2 diabetes, type 1 diabetes, cystic fibrosis, and in infants, especially those with neonatal diabetes. Medications such as corticosteroids and atypical antipsychotics can precipitateHHS.

DKA and HHS may overlap and particular care in the assessment is needed to diagnose such a condition so that modification in management can be done to address the associated biochemical disturbances.

Hyperosmolar Hyperglycaemic State (HHS) requires different treatment. Differences in treatment strategy between HHS and DKA include the volume of fluid administered, the timing of insulin administration, and monitoring of the decline in corrected serum sodium concentration.

 

➡️Causes of DKA (severe insulin deficiency and increased level of counter-regulatory hormones):

▪️ In newly diagnosed patients, DKA is frequently the consequence of a delay in diagnosis (E)

▪️ In children with established diabetes most cases are due to insulin omission (especially basal component) or interruption of insulin delivery in children using insulin pumps. A minority of DKA cases in these children are caused by infection (mostly avoidable if sick day rules are followed).

▪️  Simply eating high carbohydrate diet does NOT cause DKA.

➡️Therapy of DKA

The child with DKA should receive care in a unit that has:

▪️ Experienced nursing (with one-to-one nursing) and medical staff trained in pediatric DKA management who are available to perform meticulous monitoring until DKA has resolved.

▪️ Clinical practice guidelines. Staff should have access to clinical practice guidelines in written or electronic format.

▪️ Access to a laboratory that can provide frequent and timely Lab results.

▪️ Whenever possible, a specialist/consultant pediatrician with expertise in the management of DKA should direct patient management. (E)

▪️ Goals of therapy:

  • To correct dehydration
  • To correct acidosis (caused mainly by volume depletion followed by insulin deficiency and increase in ketone bodies, free amino acids and free fatty acids in blood. Lactic acidosis due to tissue hypoperfusion may also contribute to the acidosis)
  • To reverse ketosis
  • To gradually restore hyperosmolality and blood glucose concentration to near normal
  • To monitor for acute complications
  • To identify and treat any precipitating event.

Estimation of the degree of dehydration in DKA is imprecise (dehydration in DKA is hyperosmolar  dehydration) and may vary among examiners.

  • Mild: pH < 7.3 or serum bicarbonate <18 mmol/L.
  • Moderate: pH < 7.2 or serum bicarbonate <10 mmol/L.
  • Severe: pH < 7.1 or serum bicarbonate <5 mmol/L.

 

Laboratory measures have been found to be better predictors of dehydration severity than clinical signs. These include:

o   Higher serum urea nitrogen (>20 mg/dl)

o   Lower pH (<7.1)

  • Wide anion gap
  • ≥10% dehydration is suggested by the presence of weak or impalpable peripheral pulses, hypotension or oliguria.

Mild DKA assumes 5%, moderate DKA 7% and severe DKA 10% dehydration.

 

Hypertension occurs in 12% of children with DKA at presentation and develops during treatment in an additional 16%. It should not be considered sign for cerebral injuy in the absence of other signs.

           

➡️Causes of Morbidity and Mortality of DKA (Complications): (ISPAD 2022)

•        Mortality is mainly due to cerebral injury.

•        It is infrequent to have permanent severe neurological sequelae resulting from DKA related brain injuries.

•        Renal tubular damage (RTD) and acute kidney injury (AKI) are more common in children with severe acidosis and volume depletion (AKI Stage 1, 2, or 3 is defined by serum creatinine 1.5, 2, or 3 times estimated baseline creatinine). They are managed by restoration of fluid volume and correction of acidosis.

➡️Other complications include:

•  Hypokalemia * (potassium may decrease rapidly during treatment, predisposing to cardiac arrhythmias. Severe hypokalemia below 2.5 meq/l is an independent marker of mortality). Potassium replacement is required regardless of the serum potassium concentration, except if renal failure is present).

•  Hypoglycemia

•  Hypocalcemia, hypomagnesemia

•Severe hypophosphatemia *

• Hyperchloremic acidosis

•  Hypochloremic alkalosis

•   Other central nervous system complications including cerebral venous sinus thrombosis, basilar artery thrombosis, intracranial hemorrhage, cerebral infarction

•   Deep venous thrombosis *

• Pulmonary embolism *

•  Rhinocerebral or pulmonary mucormycosis

•  Aspiration pneumonia*

•  Pulmonary edema *

•   Adult respiratory distress syndrome (ARDS)

• Prolonged QTc

• Pneumothorax, pneumomediastinum and subcutaneous emphysema

•  Rhabdomyolysis *

•  Ischemic bowel necrosis

• Renal failure*

•  Acute pancreatitis *

*= These are more frequent in HHS.

The aim of this adapted clinical practice guideline (CPG) is to provide evidence-based recommendations for the management of diabetic ketoacidosis in children and adolescents.

These recommendations were adapted from the relevant International Society for Pediatric and Adolescent Diabetes (ISPAD) Clinical Practice Consensus Guidelines 2018 and 2022 CPG(s) using a formal methodology for CPG adaptation: the Adapted-ADAPTE.

➡️Purpose and Scope

These guidelines have been developed to standardize the delivery of services and to implement the guidance on the prevention, diagnosis and management of DKA in age group 1 to 18 years old. It provides guidance to primary health care providers, pediatricians and specially trained nurses. The guidelines aimed to for use by various healthcare providers in the field namely paediatricians, diabetologists or endocrinologists, and intensivists

This version of the guideline includes recommendations and good practice statements for:

·  Diagnosis and management of DKA.

•     Prevention of Cerebral edema and HHS.