**5. Management of DKA**

### **5.1. Goals of therapy**

**4.2. Diagnosis of DKA**

296 Type 1 Diabetes

trations [19].

for HHS include [20-22]:

**◦** serum bicarbonate >15 mmol/L

**◦** small ketonuria, absent to mild ketonemia

**◦** effective serum osmolality >320 mOsm/kg

difficult to demonstrate in the very young.

relative to body mass.

**◦** arterial pH >7.30

**◦** stupor or coma

in the emergency room. Examples of such are:

Although DKA is defined by the biochemical triad of ketonemia, hyperglycemia and acide‐ mia, several exceptions do exist which may provide a diagnostic dilemma for the physician

**• "Euglycemic ketoacidosis''**: Partially treated children and children who have consumed little or no carbohydrate may present rarely with mildly increased blood glucose concen‐

**• Absent or mild metabolic acidosis, ketonemia and ketonuria**: This may occur in the Hy‐ perglycemic Hyperosmolar State (HHS) or if the patient experiences severe vomiting

**•** Hyperglycemic hyperosmolar state (HHS), also referred to as hyperosmolar nonketotic coma, may occur in young patients withT2DM, but rarely in T1DM subjects. The criteria

It is important to recognize that overlap between the characteristic features of HHS and DKA may occur. Some patients with HHS, especially when there is very severe dehydration, have mild or moderate acidosis. Conversely, some children with T1DM may have features of HHS (severe hyperglycemia) if high carbohydrate containing beverages have been used

**•** Other diagnostic difficulties may be faced in the very young age such as the following [2]:

**◦** Polyuria, polydipsia and weight loss which are characteristic features of diabetes are

**◦** up to 70% of the young have DKA as a first presentation, hence, at presentation, dura‐ tion of DKA is usually longer, dehydration and acidosis are more severe, as young chil‐ dren have relatively higher basal metabolic rate, and a relatively large surface area

**•** Measurement of blood ß-hydroxybutyrate (ß -OHB) concentration, may not be available in all labs, besides, urine Ketone testing can be misleading due the following reasons [2,4]:

**◦** The used method does not detect the major ketone body B-hydroxybutyrate. (sodium nitroprusside only measures acetoacetate and acetone). Serum ß-OHB concentrations,

which may lead to alkalosis which can mask the present acidosis.

**◦** plasma glucose concentration >33.3 mmol/L (600 mg/dL)

to quench thirst and replace urinary losses prior to diagnosis [22].

Management of DKA should be mainly directed to correction of acidosis. Immediate aims of management include [1,4]:


#### **5.2. Place of management**

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


Children with severe DKA or those at high risk for cerebral edema should be treated in an intensive care unit (pediatric, if available) or in a unit that has equivalent resources and su‐ pervision, such as a children's ward specializing in diabetes care [4].

In a child with established diabetes, whose parents have been trained in sick day manage‐ ment, and who presents with mild DKA, can be managed in an outpatient health care facili‐ ty (e.g., emergency ward), provided an experienced diabetes team supervises the care [15].

*Emergency Assessment [23]*


**•** A peripheral intravenous (IV) catheter should be placed for convenient and painless re‐ petitive blood sampling. An arterial catheter may be necessary in some critically ill pa‐

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299

**•** Perform continuous electrocardiographic monitoring to assess T-waves for evidence of

**•** Catheterize the bladder if the child is unconscious or unable to void on demand (e.g., in‐

Meticulous monitoring of the patient's clinical and biochemical response to treatment is mandatory for timely adjustments in treatment as indicated by the patient's clinical or labo‐ ratory data. Documentation on a flow chart of hour-by-hour clinical observations, IV and or‐

**•** Hourly (or more frequently as indicated) vital signs (heart rate, respiratory rate, blood

**•** Hourly (or more frequently as indicated) neurological observations for warning signs and

**◦** change in neurological status (restlessness, irritability, increased drowsiness, inconti‐ nence) or specific neurologic signs (e.g., cranial nerve palsies, abnormal pupillary re‐

**•** Hourly (or more frequently as indicated) accurate fluid input (including all oral fluid) and

**•** Capillary blood glucose should be measured hourly (but must be cross-checked against laboratory venous glucose, as capillary methods may be inaccurate in the presence of

**•** Give antibiotics to febrile patients after obtaining appropriate cultures of body fluids

**•** Give oxygen to patients with severe circulatory impairment or shock

**6. Further clinical and biochemical monitoring**

al medications, fluids, and laboratory results is very helpful.

Monitoring should include the following [4]:

**◦** inappropriate slowing of heart rate

poor peripheral circulation and acidosis).

symptoms of cerebral edema. The latter include:

pressure)

**◦** Headache

sponses)

output.

**◦** recurrence of vomiting

**◦** rising blood pressure

**◦** decreased oxygen saturation **•** Amount of administered insulin

tients managed in an intensive care unit.

fants and very ill young children)

hyper- or hypokalemia


*Biochemical assessment [1,4]*

	- **◦** Increased serum urea nitrogen and hematocrit may be useful markers of the severity of extracellular fluid (ECF) contraction.
	- **◦** It has to be noted that an elevated white blood cell count in response to stress is charac‐ teristic of DKA and is not necessarily indicative of infection [24].
	- **◦** Metabolic acidosis being an important landmark of DKA is also helpful to grade the se‐ verity of the condition and hence the prognosis by assessing its degree as follows [15]:

#### *Supportive measures [1]:*

**•** Secure the airway and empty the stomach by continuous nasogastric suction to prevent pulmonary aspiration, in case there is deterioration in conscious level.

