Clinical Features: Early warning: Shaking, trembling, sweating, paresthesis in lips and tongue, hunger, palpitations,headache.

Neuroglycopenia;

MILD: Diplopia, difficulty in concentrating, slurring of speech MODERATE: Confusion, behaviour change,

SEVERE: Restlessness with sweating, seizures, focal neurological deficits-hemiplegia (specially inelderly patients)

Prevention is most important. All DM patients should always carry sugar/ sweet food substances. Atthe onset of early warning symptoms, they should take 10-20 g of glucose immediately.

Management is by early recognition and bolus intravenous glucose 50% -50ml/25ml. Repeat bolusesmay be needed. If the patient has also been on OHA’s, IV infusion of 5% dextrose/ DNS should be considered, till 48h at least as an inpatient till the drug gets washed out of the system, with close monitoring of sugars.

Repeated attacks of hypoglycaemia warrant a look for causes of reduced need for insulin, as well asdose reduction after proper titration.

1. B. DIABETIC KETO – ACIDOSIS

Ketoacidosis results due to lack of insulin. In practice it is usually due to:

a.         Stopping Insulin/ reducing the dose- error/ deliberately;

b.        Resistance to insulin during infections/ other stresses ( acute MI, surgery, etc)

c.         Unrecognized onset of IDDM Clinical assessment:

Recognising DKA:

·       Drowsiness

·       Dehydration(5L deficit)

·       Kussmaul’s breathing

·       Hypotension

Investigations:

Confirm diagnosis by:

·       Hyperglycemia (blood glucose)

·       Ketonemia (Urine acetone)

·       Acidosis ( blood gases) Treatment:

Principles of treatment:-

1)    The plasma glucose level invariably falls more rapidly than plasma ketone level. Insulin administration should not be stopped because glucose concentrations approach normal; Insulin should be infused along with glucose with adequate potassium correction till ketonesare cleared up.

2)    The response to treatment is measured more accurately by arterial pH and onion gap rather than plasma ketone bodies which may erroneously give a rising value during the initial phaseof treatment.

Treatment of precipitating factors: Antibiotics for infection (Cefotaxime and Gentamicin) ,management of situations like MI, strokes, etc.

1.   C. NON-KETOTIC HYPEROSMOLAR COMA (NKHOC):

A metabolic emergency in which the increased blood glucose causes increase in the osmolality, causing osmotic diuresis and therefore severe dehydration in the absence of ketosis and acidosis.The lack of ketosis is due to the presence of some circulating insulin (suboptimal levels) .

Clinical assessment: Severe dehydration (approximately 10-12L of fluid deficit), obtundation of the sensorium (stupor/coma). Usually elderly; profound dehydration can predispose to hypercoagulablestate causing stroke, AMI, arterial insufficiency in the limbs.

Investigations: Increased plasma osmolality and hyperglycemia in the absence of urinary ketone bodies and a normal pH on ABG. Calculation of osmolality can be done from the values of serum Na,K, Glucose and Urea.

Formula: 2x (Na+K) + Glucose (mmol/L) + Urea (mmol/L)

Or       2x (Na+K)+0.055 x Glucose (mg%) +0.166 x Urea(mg%)

Treatment: Mostly as in DKA. The fluid deficit is more (10-12Ls); therefore to be placed carefully withQ2hly Na and K monitoring. Use 1/ 2 or 1/4 NS as serum sodium is high. Central venous pressure monitoring is absolutely essential because the volume of correction is large and the rate of replacement should be adequate. DVT prophylaxis can be considered.