You'll also be closely monitored for any life-threatening problems that can happen, such as problems with your brain, kidneys or lungs. You can leave hospital when you're well enough to eat and drink and tests show a safe level of ketones in your body. It's common to stay in hospital for around 2 days. Before leaving hospital, ask to speak to a diabetes nurse about why you got DKA and what you can do to stop it happening again.
Page last reviewed: 01 May Next review due: 01 May Diabetic ketoacidosis. It's still important to get medical help if you need it. Then you will know what to do when you are sick. Drink extra fluids to prevent dehydration. These include water, broth, and sugar-free drinks. If you don't drink enough, the insulin from your shot may not get into your blood.
So your blood sugar may go up. Try to eat as you normally do, with a focus on healthy food choices. Check your blood sugar at least every 3 to 4 hours. Check it more often if it's rising fast. If your doctor has told you to take an extra insulin dose for high blood sugar levels for example, above If you're not sure how much to take, call your doctor or nurse call line.
Check your temperature and pulse often. If your temperature goes up, call your doctor or nurse call line. You may be getting worse.
If you take insulin, check your urine or blood for ketones, especially when you have high blood sugar for example, above Call your doctor or nurse call line if your ketone level is moderate or high. If you missed your usual dose of insulin or other diabetes medicine, take the missed dose or take the amount your doctor told you to take if this happens. If you and your doctor decide on a dose of extra-fast-acting insulin, give yourself the right dose.
If you take insulin and your doctor has not told you how much fast-acting insulin to take based on your blood sugar level, call your doctor or nurse call line. Drink extra water or sugar-free drinks to prevent dehydration.
Wait 30 minutes after you take extra insulin or missed medicines. Then check your blood sugar again. If symptoms of high blood sugar get worse or your blood sugar level keeps rising, call your doctor or nurse call line. If you start to feel sleepy or confused, call For example, call if: You passed out lost consciousness. You are confused or cannot think clearly. Your blood sugar is very high or very low. Watch closely for changes in your health, and be sure to contact your doctor or nurse call line if: Your blood sugar stays outside the level your doctor set for you.
You have any problems. Current as of: August 31, The commonly used diagnostic criteria for diabetic ketoacidosis and average deficits of water and electrolytes are given in Table 1. Diabetic ketoacidosis.
Ellenberg and Rifkin's Diabetes mellitus. Stamford, Conn. Major components of the pathogenesis of diabetic ketoacidosis are reductions in effective concentrations of circulating insulin and concomitant elevations of counterregulatory hormones catecholamines, glucagon, growth hormone and cortisol. Hyperglycemia initially causes the movement of water out of cells, with subsequent intracellular dehydration, extra-cellular fluid expansion and hyponatremia.
It also leads to a diuresis in which water losses exceed sodium chloride losses. Urinary losses then lead to progressive dehydration and volume depletion, which causes diminished urine flow and greater retention of glucose in plasma. The net result of all these alterations is hyperglycemia with metabolic acidosis and an increased plasma anion gap.
The history and physical examination continue to be important aspects of management. Even in comatose patients, information documenting a history of diabetes or insulin therapy may be available. The physical examination can provide supportive evidence for the diagnosis of diabetic ketoacidosis and can point to precipitating factors Table 2. Hyperglycemic crises in urban blacks. Although usually straightforward, the diagnosis of diabetic ketoacidosis is occasionally missed in unusual situations, such as when it is the initial presentation of diabetes in infants or elderly patients or when patients present with sepsis or infarction of the brain, bowel or myocardium.
These presentations can distract the physician from the underlying diagnosis of diabetic ketoacidosis. The laboratory tests needed to confirm the presence of diabetic ketoacidosis and to screen for precipitating events are summarized in Table 1 4 and Figure 2. The essential data can be obtained promptly in the emergency department. Protocol for the management of patients with diabetic ketoacidosis.
The therapeutic goals for diabetic ketoacidosis consist of improving circulatory volume and tissue perfusion, reducing blood glucose and serum osmolality toward normal levels, clearing ketones from serum and urine at a steady rate, correcting electrolyte imbalances and identifying precipitating factors. A suggested flow sheet for monitoring therapeutic response is provided in Figure 3.
A suggested flow sheet for monitoring response to therapy for diabetic ketoacidosis. Diabetic ketoacidosis and the hyperglycemic hyperosmolar nonketotic state. Joslin's Diabetes mellitus. The severity of fluid and sodium deficits Table 1 4 is determined primarily by the duration of hyperglycemia, the level of renal function and the patient's fluid intake.
Dehydration can be estimated by clinical examination and by calculating total serum osmolality and the corrected serum sodium concentration. Total serum osmolality is calculated using the following equation:.
The measured serum sodium concentration can be corrected for the changes related to hyperglycemia by adding 1. The initial priority in the treatment of diabetic ketoacidosis is the restoration of extra-cellular fluid volume through the intravenous administration of a normal saline 0. This step will restore intravascular volume, decrease counterregulatory hormones and lower the blood glucose level. In patients with mild to moderate volume depletion, infusion rates of 7 mL per kg per hour have been as efficacious as infusion rates of 14 mL per kg per hour.
When the blood glucose concentration is approximately mg per dL This allows continued insulin administration until ketonemia is controlled and also helps to avoid iatrogenic hypoglycemia. Another important aspect of rehydration therapy in patients with diabetic ketoacidosis is the replacement of ongoing urinary losses.
Modern management of diabetic ketoacidosis has emphasized the use of lower doses of insulin. This has been shown to be the most efficacious treatment in both children and adults with diabetic ketoacidosis. It is prudent to withhold insulin therapy until the serum potassium concentration has been determined. In the rare patient who presents with hypokalemia, insulin therapy may worsen the hypokalemia and precipitate life-threatening cardiac arrhythmias. Standard low-dose insulin therapy consists of an initial intravenous bolus of 0.
In clinical situations in which continuous intravenous insulin cannot be administered, the recommended initial insulin dose is 0. Subsequently, regular insulin should be given in a dosage of 0. If the blood glucose concentration does not fall by 50 to 70 mg per dL 2. Either of these treatments should be continued until the blood glucose level falls by 50 to 70 mg per dL. Low-dose insulin therapy typically produces a linear fall in the glucose concentration of 50 to 70 mg per dL per hour.
More rapid correction of hyperglycemia should be avoided because it may increase the risk of cerebral edema. This dreaded treatment complication occurs in approximately 1 percent of children with diabetic ketoacidosis. Cerebral edema is associated with a mortality rate of up to 70 percent. When a blood glucose concentration of mg per dL has been achieved, the continuous or hourly insulin dosage can be reduced to 0. The insulin and fluid regimens are continued until ketoacidosis is controlled.
This requires the achievement of at least two of these acid-base parameters: a serum bicarbonate concentration of greater than 18 mEq per L, a venous pH of 7. Although the typical potassium deficit in diabetic ketoacidosis is to mEq to mmol , most patients are hyperkalemic at the time of diagnosis because of the effects of insulinopenia, hyperosmolality and acidemia.
One protocol entails using insulin and intravenous fluids until the serum potassium concentration is less than 5. At this time, potassium chloride is added to intravenous fluids in the amount of 20 to 40 mEq per L.
The exact amount of potassium that is administered depends on the serum potassium concentration. When the serum potassium level is less than 3. If the serum potassium is greater than 3. The goal is to maintain the serum potassium concentration in the range of 4 to 5 mEq per L 4 to 5 mmol per L. In general, supplemental bicarbonate therapy is no longer recommended for patients with diabetic ketoacidosis, because the plasma bicarbonate concentration increases with insulin therapy.
Retrospective reviews and prospective randomized studies have failed to identify changes in morbidity or mortality with sodium bicarbonate therapy in patients who presented with a pH of 6.
Therefore, the use of bicarbonate in a patient with a pH greater than 7. Furthermore, bicarbonate therapy carries some risks, including hypokalemia with overly rapid administration, paradoxic cerebrospinal fluid acidosis and hypoxia. Some authorities, however, recommend bicarbonate administration when the pH is less than 7. If bicarbonate is used, it should be given as a nearly isotonic solution, which can be approximated by the addition of one ampule of sodium bicarbonate in mL of sterile water.
The bicarbonate solution is administered over a one-hour period. A small percentage of patients who have diabetic ketoacidosis present with metabolic acidosis and a normal anion gap. Therefore, they have fewer ketones available for the regeneration of bicarbonate during insulin administration.
Osmotic diuresis leads to increased urinary phosphate losses. During insulin therapy, phosphate reenters the intracellular compartment, leading to mild to moderate reductions in the serum phosphate concentration. Adverse complications of hypophosphatemia are uncommon and occur primarily in patients with severe hypophosphatemia a serum phosphate concentration of less than 1. Prospective studies have indicated no clinical benefit for phosphate replacement in the treatment of diabetic ketoacidosis, and excessive phosphate replacement may contribute to hypocalcemia and soft tissue metastatic calcification.
One protocol is to administer two thirds of the potassium as potassium chloride and one third as potassium phosphate.
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