With respect to diabetic ketoacidosis (DKA), which ONE of the following statements is TRUE?
Answer: B: The standard urine ward test using test strips detects only acetoacetate as ketones but not beta-hydroxybutyrate. Blood or serum should be tested to detect both types of ketones. This can be performed at the bedside using special test strips or in the laboratory. Measuring both types of ketones is important for monitoring the response to insulin therapy in DKA. Insulin infusion should be continued until ketones are completely cleared from blood and the AG is normalized. The majority of DKA patients present with metabolic acidosis with a wide AG due to ketonaemia. However, some patients may present with compensatory metabolic alkalosis with normal or high HCO3 levels. In these patients a wide AG is still present due to ketonaemia. Kussmaul hyperventilation is a compensatory respiratory reflex induced by severe metabolic acidosis. In DKA, there are increased renal losses of important electrolytes (sodium, chloride, potassium, calcium, magnesium and phosphate) due to the high osmotic load provided by hyperglycaemia. Acidaemia increases renal losses of potassium ion (K+ ), further depleting the total body K+ . However, acidaemia pushes intracellular potassium to the extracellular space, which can result in initial normal or high serum K+ level. When volume depletion is corrected and acidaemia improved with treatment, hypokalaemia develops unless potassium is adequately replaced.
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Regarding the management of DKA, which ONE of the following statements is TRUE?
Answer: B: The main priority in the treatment of DKA is to replace the total body water deficit, which averages 5–10 L (100 mL/kg) in an average adult. It is recommended that 50% of this volume is replaced within the first 12 hours and the rest during the next 12 hours.
A loading dose of insulin is not recommended for use in children and is optional in adults. In the majority of patients, initial serum K+ level is either normal or elevated despite the gross depletion of total body potassium. This is mainly due to total body water depletion and movement of potassium ions to the extracellular space secondary to acidosis.
Consequently, initial hypokalaemia means there is a severe depletion of total body potassium, and acidosis and water depletion have not been able to increase the serum K+ concentration. Initial hypokalaemia < 3.5–4.0 mmol/l should be aggressively corrected before commencement of insulin therapy. Initial hypokalaemia does not indicate less severe disease process.
Correction of the metabolic problem will normally correct the associated acid–base disorder. Sodium bicarbonate is not recommended to correct acidosis except in a limited subset of patients including patients who are critically unwell with arterial pH < 6.9 (severe acidaemia).
Regarding complications that may occur due to treatment of DKA, all of the following are true EXCEPT:
Answer: C: Cerebral oedema is a serious complication that occurs (especially in children) during treatment of DKA. It has a mortality risk of 70% once developed, with 10% of survivors having permanent neurological sequelae. Cerebral oedema usually develops when it appears to be having clinical and biochemical improvement in the child. However, at that point the child develops mainly neurological signs and symptoms. These include:
Cerebral oedema is a clinical diagnosis. Immediate treatment with intravenous mannitol is indicated to prevent potential serious consequences.
Intubation and ventilation are required to control rising intracerebral pressure. A head CT can be performed once mannitol is given. Specific risk factors associated with the development of cerebral oedema include:
There is no evidence to suggest increased volume replacement, sodium-containing fluids, or rate of fall of blood glucose cause cerebral oedema. Rapid volume expansion during treatment improves glomerular filtration rate (GFR) and urine output. In the kidneys, this increases ketone excretion with an increase in chloride reabsorption (as HCO3 is low). This may cause hyperchloraemic acidosis with a normal AG, and hypophosphataemia. As described in answer 7, correction of fluid depletion and acidaemia without adequate supplementation may also cause rapid development of severe hypokalaemia.
Regarding hyperglycaemic hyperosmolar state (HHS), which ONE of the following statements is TRUE?
Answer: A: HHS presents most commonly in elderly, poorly controlled or undiagnosed type 2 diabetes patients. It often develops insidiously over days or weeks after a variety of serious illnesses. These patients often have multiple comorbidities and lack capacity to communicate. They may have limited ability to access water intake freely. All these factors may contribute to the higher mortality seen in HHS. In HHS, blood glucose levels are often much higher than seen in DKA, often >60 mmol/L.
There is severe total body water (TBW) contraction secondary to losses caused by osmotic diuresis due to severe hyperglycaemia in the face of severely restricted access to free water intake. TBW loss may reach 8–10 L in an average adult (compared with 5–6 L in DKA). Therefore calculated serum osmolality is often >315 mmol/L. Arterial pH usually remains >7.3, although wide AG metabolic acidosis may develop during the course of disease. This is mainly due to hypoperfusion of tissues and may be contributed by starvation ketosis. The ketone bodies remain small in amount and do not significantly contribute to acidosis.
In the management of HHS, which ONE of the following statements is TRUE?
Answer: D: HHS patients are significantly dehydrated and poorly mobile, and may develop disseminated intravascular coagulation. Thromboembolic risk is therefore high, and so heparin prophylaxis should be initiated at an early point.
These patients are usually sensitive to insulin, with insulin resistance being quite uncommon. Higher doses are usually not required. Insulin therapy should be started only after adequate volume repletion and correction of hypokalaemia. Adequate volume replacement prior to administration of insulin in HHS prevents cardiovascular collapse, caused by a sudden intracellular fluid shift that accompanies the intracellular glucose movement induced by insulin. Insulin should therefore be administered cautiously to produce a slow fall in blood glucose. While total body potassium deficits are significant, the initial serum level may be normal in the face of severe volume contraction. Insulin therapy will result in the intracellular movement of potassium causing hypokalaemia, so replacement will generally be required at an early stage.
In HHS there is a total body sodium deficit. However, initial corrected serum sodium may be low, normal or high, depending on the degree of volume depletion. Hyper-natraemia along with very high serum osmolality, are poor prognostic factors and correspond to severe volume depletion. Fluid replacement, guided by central venous pressure (CVP) monitoring if necessary, should aim first to correct hypotension, then to slowly replace water deficit over a period of several days.
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