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Absence of a Relation between Lipogenesis and Ketogenesis in vivo. Nature , — Download citation. Issue Date : 21 February Anyone you share the following link with will be able to read this content:. Ampoules of phosphate available in my hospital contain about 15 mmoles of phosphate and 20 mmoles of potassium and one ampoule can be diluted in the IV fluids and infused over an hour.
Sodium bicarbonate in DKA has arguably a minor role is in urgent management of serious arrhythmias due to hyperkalaemia in DKA. However, glucose-insulin is the preferred treatment in this patient group. None of the studies done in DKA have shown any benefit of bicarbonate treatment. Potential problems are sodium overload, CSF acidosis, intracellular acidosis, exacerbation of hypokalaemia, rebound alkalosis and impaired tissue oxygen delivery shift of oxyhaemoglobin dissociation curve. After treatment of DKA starts, the slowest biochemical parameter to recover is usually the serum bicarbonate - this is especially so when substantial amounts of ketones have been lost in the urine.
New bicarbonate is generated when the condition is reversed and the ketones are metabolised. Bicarbonate administration is not necessary. Monitoring should include observations of airway, breathing, circulation and level of consciousness, serial blood gases and electrolytes, urinary ketones and urine output. Serum lactate is occasionally useful. A Biochemistry Flowchart of results is strongly recommended. Cerebral oedema is the commonest single cause of mortality, particularly in children.
It typically develops after treatment has commenced. A headache or decreasing level of consciousness are the usual initial sign.
Onset may be sudden. Treat urgently with IV mannitol. Intubation for airway protection may be required. Maintain hyperventilation in ventilated patients. The commonest precipitants in young diabetics are inadequate insulin eg first presentation of diabetes, omission of doses and infection.
Often no specific cause can be found. In older diabetics, DKA may be precipitated by a major medical illness esp infection. Antibiotics or surgical management are necessary in some cases. Patient education to prevent further episodes is very important.
Pathophysiology The poor oral intake results in decreased glycogen stores, a decrease in insulin levels and an increase in glucagon levels. Other points to note: Volume depletion is common and this can result in increased levels of counter-regulatory hormones eg glucagon Levels of FFA can be high eg up to 3.
Management This syndrome is rapidly reversed by administration of glucose and insulin. Lebovitz, An outline of the pathophysiology is presented below. The pathogenesis requires two events: Increased mobilisation of free fatty acids FFA from adipose tissue to the liver A switch of hepatic lipid metabolism to ketogenesis FFA mobilisation is initiated by the effect of absolute or relative insulin deficiency on fat cells. The hepatic effects of a fall in the insulin:glucagon ratio are: Increased glycogenolysis Increased gluconeogenesis Increased ketogenesis The net effect is an increase in the hepatic output of both ketone bodies and glucose.
Why does the major switch in hepatic metabolism occur? Development of hyperchloraemic acidosis In some cases, a hyperchloraemic metabolic acidosis develops: this is most common during the treatment phase. Other acid base disorders may be present It should not just be assumed that the patient only has a diabetic ketoacidosis.
Possible complicating acid-base disorders are: Lactic acidosis due to hypoperfusion and anaerobic muscle metabolism Metabolic alkalosis secondary to excessive vomiting Respiratory acidosis due to pneumonia or mental obtundation Respiratory alkalosis with sepsis Renal tubular acidosis type 4 Renal tubular acidosis type 4 is present in some diabetic patients and the associated urinary acidification defect can cause a hyperchloraemic normal anion gap acidosis.
Summary of Events in Pathophysiology of DKA First: A precipitating event occurs which results in insulin deficiency absolute or relative and usually an excess of stress hormones particularly glucagon Hyperglycaemia occurs due to decreased glucose uptake in fat and muscle cells due to insulin deficiency Lipolysis in fat cells now occurs promoted by the insulin deficiency releasing FFA into the blood Elevated FFA levels provide substrate to the liver A switch in hepatic lipid metabolism occurs due to the insulin deficiency and the glucagon excess, so the excess FFA is metabolised resulting in excess production of acetyl CoA.
The excess hepatic acetyl CoA is converted to acetoacetate a keto-acid which is released into the blood Ketoacidosis and hyperglycaemia both occur due to the lack of insulin and the increase in glucagon and most of the clinical effects follow from these two factors Other acid-base and electrolyte disorders may develop as a consequence and complicate the clinical condition.
Overall aims of treatment Replace fluid and electrolyte losses Restore normal carbohydrate and lipid metabolism Treat the underlying cause Manage specific complications Management can be considered in terms of emergency and routine components. Emergency Management A: Airway Protect by intubation with a cuffed tube if patient is significantly obtunded. Consider placing a nasogastric tube in all patients.
B: Breathing Oxygen by mask initially in all patients Intubation may be necessary for airway protection or ventilation eg if aspiration, coma, pneumonia, pulmonary oedema, acute pancreatitis and ARDS but this is not common. Special Danger in Ventilated Patients Maintain compensatory hyperventilation in intubated patients Patients with metabolic acidosis eg severe DKA have marked hyperventilation ie respiratory compensation, Kussmaul respirations and typically low arterial pCO 2 levels.
If this is not done and pCO 2 is inappropriately high, a severe acidaemia and consequent severe cardiovascular collapse may occur This is a particular problem in all situations where a patient with a compensated metabolic acidosis is intubated and ventilated.
C: Circulation If shock is present, this requires urgent colloid infusion to restore intravascular volume and tissue perfusion Arrhythmias require urgent clinical management dependent on the type and the clinical situation eg hyperkalaemia, myocardial infarction The typical patient who presents with poor peripheral perfusion but normotension can be adequately managed initially with ECF replacement fluids eg Hartmann's solution or Normal saline.
DKA : Routine Management 1. General Oxygen by mask Urinary catheter Consider low dose calcium heparin to decrease risk of arterial thrombosis Investigate for underlying illness history, examination, cultures of blood, urine or sputum, chest xray, ECG etc.
Fluids Immediate aim is to restore intravascular volume to improve tissue perfusion. Potassium Serum level is commonly normal or high due to the acidosis at presentation despite the presence of a large total body potassium deficit due to renal losses. Insulin Fluid resuscitation is necessary to deliver insulin to its sites of action in liver, muscle and adipose tissue. Phosphate Though a total body deficiency is always present, it has not been possible to show that acute phosphate administration makes any difference to outcome.
Bicarbonate Sodium bicarbonate in DKA has arguably a minor role is in urgent management of serious arrhythmias due to hyperkalaemia in DKA. Ketone testing is an essential part of managing diabetes. High ketone levels can be dangerous, and may lead to ketoacidosis. Find out when, how, and…. Ketosis is a metabolic process in which the body burns stored fat for energy, instead of glucose.
Some people try to induce ketosis with a low carb…. Differences between ketosis and ketoacidosis. Medically reviewed by Debra Sullivan, Ph. Ketosis vs. Share on Pinterest A doctor may recommend blood or urine tests to determine if someone is experiencing ketosis or ketoacidosis.
Symptoms of ketoacidosis. Symptoms of ketosis. Share on Pinterest Symptoms of ketosis may include fatigue, feeling cold, and general weakness. When to see a doctor. Treatment of ketoacidosis. Prevention of ketoacidosis. Share on Pinterest Monitoring blood glucose levels can help prevent ketoacidosis.
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