Dm

Dr. Mohammed khalid

Hyperglycemic – hyper Osmolar State

This condition is describe by severe hyper-glucaemia (30mmol/L (600 mg /dL)), with out significant hyper ketonaemia or acidosis.
Severe dehydration and pre renal uremia are common. It is usually affect elderly patient. Many with previously undiagnosed diabetes. It is carry high mortality rate (40%). The treatment differ from keto-aci-dosis is two main respect: First, the patients are more sensitive to insulin, they required half dose of insulin (1-3 units)/hr.

Secondly, the plasma osmolarity should be measured. It can be calculated by using this formula:
Plasma osmolarity = 2(Na+) + 2(K+) + Blood glucose + Blood urea {All in mmol/L/Kg}
The conscious is depressed when it is high 0340mmol/L/Kg
Normal value ((280-300) mmmol/L/Kg)).
The patient should be given 0.45% of saline until the osmolarity approach normal when isotonic saline (0.9%) should be substituted.
Thrombo-embolic complications are common and heparin should be given 1cc(5000u)x 2 S.C

Lactic Acidosis

The coma in lactic acidosis is likely to be in diabetic patient on Metformin therapy, for type II DM. the patient is very ill and over breathing (severe acidosis) but not profoundly dehydrated, like in diabolic keto-acidosis, and the patient smell does not smell of acetone and ketone urea is mild or even absent. The plasma bicarbonate and pH are markedly reduced (severe acidosis) (pH7.2) and the anion gap is increased. The diagnosis is confirm by high dose of lactic acid (5.0mmol/l) in the blood.
The treatment with I.V. sodium bicarbonate sufficient to raise the arterial Ph above 7.2 along with ansulin and glucose. Mortality is high 50% in spite of treatment.


hypoglycemia
Hypoglycemia is usually occur in person with diabetes treated by insulin therapy or less with sulphonyl urea drugs.
The blood glucose (3.5mmol/l (63 mg/dl) and very rarely with Metformin therapy:

Clinical assessment:-

The main common symptoms of hypoglycemia are comprise in two main groups:-
• Those related to acute activation of autonomic nervous system.
• Those secondary to glucose deprivation of the brain (Neuro-glycopenia)
• Autonomic symptoms include: Sweating – palpitation, feeling of hunger anxiety, pounding heart and trembling.

• Neuro-glycopenic symptoms:

• Confusion, drowsiness, speech difficulty in coordination, inability to concentrate in severe hyperglycemia may lead to convulsion T.1.A- stroke and even coma.
• Other non specific symptoms includes, headache, nausea and tiredness.

Impaired awareness of symptoms:-

In most instance the patient has no difficulty in recognizing the symptoms of hypoglycemia and can take approximate remedial action.
In certain circumstances eg. (during sleep, lying supine or distractive by other activities, warning symptoms are not always perceived by the patient so that appropriate action is not taken and neuroglycopenia with reduce consciousness ensues (take place).

When short acting insulin given in non-diabetic persons, symptoms of hypoglycemia appear when the venous blood glucose falls to 2.5-3mmol/L (45-54)mg/dl. In diabetic patient who is chronically hyperglycemic, the same symptoms may develop at high blood glucose level conversely patient who had strict glycaemic control and who exposed to frequent attacks of hypoglycemia may not experience of any symptoms even when the blood glucose fall below 2.5 mmol (45mg/dl).

The glycaemic threshold for the onset of symptoms and the counter-regulatory hormones secretion are altered in patient with impaired awareness of hypoglycemia.
In that the blood glucose has fall to a much lower level to trigger these response.
In that the blood glucose has fall to a much lower level to trigger these responses.
This will increased with duration of insulin treatment 50% of patient of type I DM are affected by 20 years of diabetes and this chronic form of impaired hypoglycemic.
Awareness may not be reversible, and severe hypoglycemia may be six fold increased and intensive insulin therapy should be avoided.


Deficient of counter-regularity hormones responses:-
Normally when there is falling blood glucose there is increased secretion of counter regulatory hormones which antagonize the blood glucose lowering effect of insulin.
Glucagon and adrenaline are the most potent of these. Hypoglycemia induced secretion of glucagons become impaired in most patients with in five years of developing type I DM.

After several years many patients develop defective of adrenaline response to hypoglycemia, so that if hypoglycemia develop, glucose recovery may be seriously compromised.

Causes of hypoglycemia

• Miss delayed or inadequate meal.
• Unexpected or unusual exercise.
• Alcohol
• Errors in insulin dose or in oral hypoglycemic agents or in administration.
• Lipo hypertrophy.
• Gastro-paresis.
• Unrecognized other endocrine disorder eg. Addison’s disease.
• Dumping syndrome.

Severe hypoglycemia

• Define as: Hypoglycemia requiring the assistance of another person for recovery and carry serious morbidity and (2-4%) of mortality ratio and it may lead to repeated convulsion, T.I.A., stroke, arthymia, and myocardial ischemia and brain damage.
• The following are the risk factors for severe hypoglycemia:
• Strict glycemic control.
• Impaired awareness of hypoglycemia.
• Sleep
• Age (very young-elderly)
• History of previous hypoglycemia.
• Increase duration of diabetes.
• Renal and hepatic impairment.


management
• The treatment of hypoglycemia depend on severity of hypoglycemia and whether the patient is conscious and able to swallow.
• If hypoglycemia is recognized early and the patient is conscious. It can be resolved by oral carbohydrate like glucose tablet, drink or by a jam, honey, put in the buccal area. But if the patient is unable to swallow or unconscious is treated by: I.V. 50% of glucose (30-50ml), followed by 10% glucose infusion for the next 24 hr. (10gm/hr), to prevent another attack of hypoglycemia.

• Or: can be treated 1mg of glucagons I.M.

• Full recovery may not be occur immediately until 60-90min, after normo-glycaemia is restored.
• The development of cerebral oedema should be considal in patient who fail to regain his consciousness after blood glucose return to normal and should be treated by high concentrated of oxygen and 20% of monitol 1gm/kg infusion.
• If the patient return his consciousness look for the underlining cause and for any risk factors.
• Unless the reason for hypoglycemic episode is clear the next dose of insulin should be reduced by 20% of the previous dose.