Nursing management of a patient with diabetic ketoacidosis

INTERNATIONAL

- incidence is not known but may be higher in developing countries. RACE - incidence is higher in whites because of higher incidence of type1diabetes in this racial group. SEX - common in females than in males. AGE - individuals <19yrs. persons with diabetes at any age.

Mortality/Morbidity
2% per episode o before discovery of insulin in 1922 the mortality rate was 100% o best results with patient treated in ICU during first two days of hospitalization. o in contrast mortality rate is still high in developing countries and among non hospitalized patients.
o

Definition
Diabetic ketoacidosis is defined clinically as an acute state of severe uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids. DKA is defined biochemically as an increase in the serum concentration of ketones greater than 5mEq/L, a blood glucose level of greater than 250mg/dl, blood pH of less than 7.2 and a biocarbonate level of 18mEq/L or less.

CAUSES OF DKA

PATIENTS WITH TYPE1 DIABETES

PATIENTS WITH TYPE2 DIABETES

acute insulin deficiency poor compliance with insulin psychological stress or lack of education bacterial infection intercurrent illness medical, surigal, or emotional stress brittle diabetes idiopathic anti insulin factors Insulin infusion catheter blockage mechanical failure of insulin infusion pump. intercurrent illness medications

Pathophysiology of DKA
Absolute/relative

insulin deficiency

in counterregulatory hormones. + (glucagon, cortisol,growth hormone,epinephrine) Hormonal imbalance

Increase

Enhances gluconeogenesis , glucogenolysis

(lipolysis)

 Severe

Increases

hyperglycaemia renal threshold of glucose absorption & results in significant glycosuria. water loss in urin due to osmotic diuresis, dehydration,acidosis.

serum fattyacids. hepatic metabolism of fattyacids.

Exceeds

Increases

ketogenesis. Results in intermediate

and end metabolites. (ketones & ketoacids)

Severe

Acetone produces ketotic breath Betahydroxybutyrate Induces nausea & vomiting Increases fluid electrolyte loss.

Acetoacetate Progressive rise of blood concentration of these acidic organic substances. leads to

State of ketonemia.

Natural body buffers can buffer ketonemia in early stage. Accumulated ketones exceed bodys capacity of extracting them, they overflow into urine.

i.e, ketonuria.

If not treated promptly.

More accumulation of organic acids leads to frank clinical metabolic acidosis. i.e, ketoacidosis

Ph

HCO3 LEVEL

Respiratory compensation of this acidotic condition. KUSSMAUL RESPIRATION.

Clinical features of DKA

POLYURIA, POLYDIPSIA, POLYPHAGIA. NAUSEA, VOMITING. DIFFUSED ABDOMINAL PAIN. GENERALISED WEAKNESS. ALTERED SENSORIUM. FLU LIKE SYMPTOMS. KETOTIC BREATH. HYPERVENTILATION. EXTREME WT LOSS. MUSLE WASTING. ACUTE CHEST PAIN OR PALPITATION . PAINLESS INFARCTION. H/O MISSING INSULIN DOSE. H/O RAPID WT LOSSIN PTS WHO ARE NEWLY DIAGNOSED TYPE 1 DIABETES MELLITUS. SIGNS OF DEHYDRATION. SIGNS OF ACIDOSIS. SIGNSOF INTERCURRENT ILLNESS.

Lab studies
Complete

blood cell count Blood glucose levels >250mg/dl Sodium decreases Potassium increases HCO3 levels assess degree of acidosis ABG levels pH is often <7.3 Ketones ketostics & uristix is used to measure ketone bodies in urine. Urine analysis to look glycosuria & underlying urinary infection. Chest radiography CT scan ECG

MANAGEMENT OF DKA
THERAPEUTIC
To

GOALS FOR DKA:-

improve circulatory volume and tissue perfusion. To reduce blood glucose and serum osmolality towards normal levels with insulin. To clear ketones from serum and urine at steady rate. To correct electrolyte imbalance, particularly potassium loss. To indentify precipitating factors. To correct acid-base balance. To treat concurrent infection. To provide immediate hyperglycemic care. To prevent complications.

Correction of fluid loss with iv fluids

FLUIDS

sodium or by ringer lactate. administer 1lt over the first 30 minutes. administer 1lt over the 2nd hour. administer 1lt over the following 2hrs. administer 1lt every 4hrs. euvolemic or hypernatremic switch to half the isotonic sodium chloride solution. When blood sugar falls less than 180mg/dl, saline is replaced with 5-10% dextrose with half isotonic saline.

To correct hyperglycemia with insulin

A low dose insulin regime has the advantage of not inducing severe hypoglycemia or hypokalemia. Only short acting insulin is used for correction of hyperglycemia. Insulin dose 0.1u/kg/hr. 6u/hr until the blood sugar drops to less than 180mg/dl. The rate of infusion decreases to 2-3u/hr until the ketoacidotic state abates. The optimal rate of glucose decline is 100mg/dl/hr. Do not allow the blood glucose level to fall below 200mg/dl during first 4-5hrs of treatment. Hypoglycemia may develop rapidly with correction of acidosis. Rebound hyperglycemia which requires long duration treatment. May induce cerebral oedema.

To correct electrolyte imbalance

potassium K

level >6meq/l do not administer k supplement. K level 4.5 to 5meq/l administer 10meq/l of kcl. K level 3-4.5meq/l administer 20 meq/l of kcl. Monitor serum k levels hrly, and stop infusion if k level is >5meq/l. Continue monitoring serum k levels to prevent recurrence of hypokalemia. In case of severe hypokalemia do not start insulin therapy to avoid severe cardiac dysrhythmias.

To correct acid-base balance

Sodiumbicarbonate

only is infused if decompensated acidosis starts to threaten the pts life. Especially when associated with sepsis or lactic acidosis. If sodiumbicarbonate is indicated 100150ml of 1.4% conc is infused initially. This MAY be repeated every half hour if necessary. Rapid and early correction of acidosis with sodiumbicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis.

To treat concurrent infection

In

the presence of infection, administer proper antibiotics guided by the results of culture and sensitivity studies. Starting emperic antibiotics on suspicion of infection until culture results are available may be advisable.

Immediate post hyperglycemic care

When DKA has been controlled, s/c insulin can be started. Administer s/c dose of regular insulin 1hr before discontinuing iv insulin. In pts who are unable to eat, 5% dextrose in hypotonic saline is continued @100-200ml/hr. Monitor blood glucose levels every 4hrly and administer insulin s/c as per sliding scale. When pts are able to eat, multidose subcutaneous therapy with both regular (short-acting) & intermediate acting insulin may be given. Newly diagnosed diabetes 0.6-0.7u/kg/day insulin is adequate to achieve metabolic control. Known diabetes pts can be given the same dose they had been receiving.

Complications of DKA
HYPOGLYCEMIA. HYPOKALEMIA. RECURRENT

HYPERGLYCEMIA. CEREBRAL OEDEMA. KETOACIDEMIA. FLUID @ ELECTROLYTE DEPLETION. ASPIRATION. PULMONARY OEDEMA. MYOCARDIAL INFARCTION. ARDS. UNRECOGNISED RENAL TUBULAR NECROSIS. HYPERCHLOREMIC METABOLIC ACIDOSIS.

Strategies to prevent diabetic ketoacidosis

Diabetic

education. Blood glucose monitoring. Sick-day management. Home monitoring of ketones or betahydroxybutyrate. Supplement short-acting insulins. Easily digestible liquid diets when. Reducing, rather than eliminating, insulin when patients are not eating. Guidelines for when patients should seek medical attention. Case monitoring of high-risk patients. Special education for patients on pump management.

s.karthi