What is the best treatment for ketoacidosis
Ketoacidosis and coma
Ketoacidosis and hyperosmolar coma are serious acute complications of diabetes mellitus. Diabetic ketoacidosis primarily affects people with type 1 diabetes who are completely insulin-deficient, while hyperosmolar coma is a complication of people with type 2 diabetes. In both cases there is a sharp increase in blood sugar above 300 mg / dl.
The exact definition of diabetic ketoacidosis, according to the S3 guideline for type 1 diabetes, is summarized in the yellow box. The prevalence of diabetic ketoacidosis is estimated to be 8-9%. The main causes are insulin-deficient conditions. This can be the case in the context of the first manifestation of type 1 diabetes or when an ongoing insulin therapy is interrupted in insulin-treated type 1 diabetics. Reasons for incorrect insulin administration can be technical reasons, e.g. B. clogged cannulas or malfunction of an insulin pump. Often the cause of diabetic ketoacidosis is also a sudden increase in the need for insulin in the context of a severe infection or in the context of severe, intercurrent diseases such as heart attack, stroke or undetected hyperthyroidism.
Typical symptoms of hyperglycemic derailment include confusion, visual disturbances, adynamia and muscle weakness, as well as polyuria, polydipsia, hypotension and tachycardia as signs of hypovolemia. As the disease progresses, pseudoperitonitis can occur, which is characterized by nausea and vomiting. Classically, those affected with ketoacidosis try to balance the acidic valences of the blood through deeper respiration. This leads to the so-called Kussmaul breathing as well as to the acetone odor due to the ketonemia, which smells fruity, putrid and sweet. Fig. 1 shows the development of the ketoacidotic coma, which in the worst case can be fatal. To assess the severity, it is not the blood sugar level that is decisive, but the extent of the acidotic derailment and desiccosis. One speaks of mild ketoacidosis if the pH value is higher than 7.3 and the standard bicarbonate is below 15 mmol / l. Moderate ketoacidosis has a pH below 7.2 and standard bicarbonate below 10 mmol / l, while severe ketoacidosis has a pH below 7.1 and standard bicarbonate below 5 mmol / l.
Diagnosis and differentiation
The diagnosis of diabetic ketoacidosis is easy to make. In practice, increased blood sugar and a two to three-fold positive test for ketone bodies in the urine with appropriate test strips lead to the diagnosis. If the symptoms match accordingly, an urgent emergency inpatient admission is required. In the clinic, the diagnosis is completed by a blood gas analysis as well as the determination of the serum electrolytes, the serum creatinine, the blood count and a CRP to rule out a serious infection.
- Blood glucose> 300 mg / dl (16.7 mmol / l)
- arterial pH <7.35 or venous pH <7.3
- Standard bicarbonate <15 mmol / l
- Ketonuria or ketonemia
- Vomiting and decreased consciousness
Differential diagnosis between hyperosmolar coma and ketoacidotic coma can be difficult, especially since the symptoms are similar. The differences between the two forms are that ketoacidosis usually develops quickly within 24 hours, exhibits the typical pseudoperitonism and acidotic breathing is the key.
The hyperosmolar coma, on the other hand, shows a creeping onset. The main differentiating criterion is that in hyperosmolar coma the pH value is usually above 7.3, while in ketoacidosis the pH value continues to drop.
Therapy for diabetic ketoacidosis is essentially aimed at eliminating dehydration, compensating for the insulin deficiency and carefully compensating for the electrolyte shift that occurs during ketoacidosis. Of course, the treatment also includes the therapy of the primary or coma-causing illnesses. It is important that therapy-related complications are to be avoided as part of the therapy. For this reason, the intensive monitoring of the patient with control of the vital parameters, careful fluid balance through central venous catheters and close-knit laboratory controls is essential.
Dehydration is carried out by administering physiological NaCl solution 0.9%, initially with 1,000 ml and then, depending on the central venous pressure, in a dosage of 100 - 500 ml / h. The fluid requirement in the first eight hours is 5 - 6 l and can increase to 10 l or 15% of the body weight during the entire treatment. The insulin therapy is carried out with human insulin (not insulin analogues) i. v. via a perfusor. Start with 0.1 IU / kg body weight per hour. An initial bolus of 10 IU can be administered. Insulin given intravenously has a short half-life of around 20 minutes, so it should be administered via the perfusor. This results in good controllability. The top priority is that blood sugar should not drop faster than 50-100 mg / dl per hour, otherwise there is a risk of brain edema. Blood sugar should be kept in the range of 200 mg / dl for the first 24 hours. If this accidentally falls too low, glucose i. v. are fed.
Caution: brain edema!
A goal that is too ambitious to normalize blood sugar quickly usually leads to immediate problems and even brain edema. The reason is that insulin lowers blood sugar much faster than the ketone body levels decrease. A complete compensation of acidosis takes at least 12 - 24 hours, only then should a corresponding diet and a switch to subcutaneous insulin therapy be started. As the blood sugar level drops and rehydration occurs, potassium is shifted intracellularly. Potassium intake should accordingly be started; this should be initiated at the start of the infusion therapy. If potassium levels are below 3 mmol / l, 30 - 40 mmol per hour should be administered. At potassium levels between 3 and 4 mmol / l the supply is reduced to 15-20 mmol per hour and at values between 4 and 5 mmol / l the supply should be reduced to 10-15 mmol per hour. To avoid cardiac arrhythmias, potassium should be kept high. If the potassium level has already decreased before the start of the infusion therapy, the potassium deficiency should first be compensated for before the insulin infusion is started.
Warning of sodium bicarbonate
The administration of insulin inhibits lipolysis and thus successfully combats acidosis. Correction of acidosis with sodium bicarbonate is not required at pH values of 7 and higher. The administration of 8.4% sodium bicarbonate with 50 mmol over an hour can only be considered if the pH value is less than 7, which is threatening to life. The main risk of acidosis correction with buffer solutions is the further drop in potassium and the risk of cerebral edema.
Therapy for hyperosmolar hyperglycemic syndrome
With this clinical picture, the blood sugar is often exorbitantly increased (blood sugar values over 1,000 mg / dl are not uncommon). This affects type 2 diabetics who have retained their own insulin performance, which in turn prevents lipolysis so that ketogenesis does not occur. What remains is hyperosmolarity with all its negative consequences (see Fig. 2). The main danger in therapy for hyperosmolar coma is dysequilibrium syndrome. To avoid this, the following applies to all measures to compensate for hypovolemia and hyperglycemia: proceed slowly!
Cerebral edema manifests itself through headache, vomiting, disorientation, aggressive behavior and the occurrence of cerebral cramps. With these symptoms, a cranial computed tomography should be performed immediately. Cerebral edema is a life-threatening complication, the treatment of which can be attempted by administering mannitol or hypermolar saline solution. The treatment of cerebral cramps is carried out by administering barbiturates and hyperventilation. However, no reliable data is available on this.
Conflicts of Interest: The author has not declared any.
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