Pathophysiology for A.M condition
A.M developed diabetic ketoacidosis (DKA), an acute metabolic complication that commonly occurs amongst patients with type 1 diabetes. Type 1 diabetes is characterized by insufficient insulin production due to autoimmune destruction of pancreatic β-cells leading to hyperglyceamia. These patients require insulin treatment to control the blood sugar levels to optimum if treatment is missed, the body stimulates hepatic glucose production through the metabolism of fatty acid, generating a metabolic cascade. ( Kahanovitz. L et al. 2018)
The pathophysiology of diabetes ketoacidosis evolves around insulin deficiency, increased insulin counter-regulatory hormones (cortisol, glucagon, growth hormone, and catecholamines) and peripheral insulin resistance, which leads to hyperglycemia, dehydration, ketosis, and electrolyte imbalance, all these underlie the pathophysiological metabolic cascade involved in DKA. ( GosmanovR.A et al. 2018) . Insulin deficiency inhibits the uptake of glucose by the cells to produce the cellular energy ATP. This energy demand then stimulates an increase in counter-regulatory hormones (i.e., glucagon, growth hormone, epinephrine, and cortisol) to compensate for the energy deficiency in the cells, they then stimulate an alternative energy production processes in the body, which is, hepatic gluconeogenesis, lipolysis, and glycogenolysis.
Due to deficiency in insulin,Serum levels of glycerol and free fatty acids rise because of uncontrolled lipolysis, so does alanine due to muscle catabolism, the body also produces glucagon in excess stimulating hepatic gluconeogenesis, this process involves metabolism or breakdown of non-carbohydrate substrates, the main precursors are lactate, glycerol, and amino acids(alanine and glutamine) into glucose, the process takes place in the liver. Lactate and amino acid alanine are converted into pyruvate, which then enters the mitochondrion and pyruvate carboxylase enzyme carboxylates them to oxaloacetate, which is reoxidized and decarboxylated by the decarboxylase enzyme in repeated steps of reverse glycolysis in the gluconeogenic pathway to yield glucose. Gluconeogenesis, coupled with decreased glucose uptake by peripheral tissues due to insulin deficiency results into hyperglycemia and increased serum circulation of free fatty acids.
Glucagon stimulates the mitochondrial conversion
Glucagon also stimulates the mitochondrial conversion of free fatty acids into ketones through ketoneogenesis which is always inhibited by insulin. High levels of acetyl coenzyme A present in the cell inhibit the pyruvate dehydrogenase complex and activates pyruvate carboxylase (Rui, 2014). These lead to a progressive rise of serum acidic concentration and ketonemia throughover production of ketone bodies and ketoacids as end metabolites that includes acetone, beta-hydroxybutyrate, and acetoacetate. Acetone is excreted via respiration and is responsible for the fruity/sweet odor, the characteristic smell in DKA, other ketones are excreted via urine and present as ketonuria on urinalysis. (Xueping Zhang, 2018)The ketoacidosis is responsible for the increased acidity by causing a significant drop in serum PH and bicarbonate levels leading to severe metabolic acidosis characterized by deep, labored fast breathing (kussmaul breathing).
Ketoneogenesis end metabolite products, in particular, beta-hydroxybutyrate, induces nausea and vomiting that consequently cause fluid and electrolyte loss already existing due to ketonuria leading to an electrolyte imbalance in DKA. Due to elevated blood sugar levels, the body struggles to excrete the excess sugar through urine by stimulating osmotic diuresis, this leads to hyperosmolarity and dehydration which in turn if not attended to leads to further electrolyte disturbance, potassium is lost through shifting of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis leading to hypokalemia. (Erika F. Brutsaert, 2019)
Serum hyperosmolarity, dehydration, and acidosis result to an increased osmolarity in the brain cells which if not attended to results to alteration in the level of consciousness. (Osama Hamdy, 2019)
Practitioners orders
The practitioner ordered A.M to be rehydrated with lactated ringers of 1000mls, this is questionable since the lab report indicated that A.M had an electrolyte disturbance with elevated potassium of 6.2, and since lactated ringers contain potassium composition of 4mEq /L it would have increased the serum potassium levels further predisposing the patient to dysarrythmia and cardiac arrest. The practitioner also ordered for furosemide 60mg IV push now, which is very questionable as the patient presented with hypotension and would have worsened the hypotension.
The choice of lab investigation was warranted since DKA is predisposed by infection and also for assessment, ABGs were appropriate to asses level of acidosis, urinalysis to asses for ketonuria. Treatment with acetaminophen was appropriate for control of fever and insulin to control the high blood sugar levels.
Urine output chart is also vital to asses the function of the kidney while rehydrating the patient.
The ideal treatment for diabetic ketoacidosis
Ideally, since DKA is characterized by hyperglyceamia, dehydration, electrolyte imbalance, and acidosis, the primary goal is to correct this deficits. Fluid rehydration is key to restore circulatory volume, using isotonic saline 0.9mmol/L is recommended but lactated ringers can be used in the setting of hypokaleamia in severe fluid loss. The recommended schedule is to administer 1-3 L during the first hour, 1 L during the second hour, another 1 L during the following 2 hours, and 1 L every 4 hours depending on the degree of dehydration and blood pressure readings. When euvolemia has been achieved, can switch the fluids to hypotonic to prevent hypernatremia, alternating of fluid with 5% dextrose is also recommended once the blood sugar levels is below 252.2mg/dl to prevent hypoglyceamia.
short-acting insulin is used for the correction of hyperglycemia. Subcutaneous absorption of insulin is reduced in DKA because of dehydration; therefore, using intravenous routes is preferable.(Hamdy . O et al 2019). regular insulin is used in an infusion of isotonic sodium chloride solution at a dose of 0.1 U/kg/hr, infused at a rate of 15 mL/h (6 U/h) until the blood glucose level drops to less than 252 mg/dL. (Osama Hamdy, 2019)
correction of electrolytes disturbance is the next approach so as prevent chronic kidney failure, potassium replacement ifpotassium. Do no administer supplement, if the potassium level is greater than 6mEq/L. If the potassium level is 4.5-6 mEq/L, administer 10mEq/h of potassium chloride. If the potassium level is 3-4.5 mEq/L, administer 20 mEq/h of potassium chloride. The potassium supplement should be started with initial fluid replacement in an infusion.
Correction of acid-base balance using sodium bicarbonate is important in restoring of normal serum PH and correcting the metabolic acidosis and is indicated when the decompensated acidosis leads to severe respiratory distress, initial infusion of 100-150 mL of 1.4% concentration is recommended.
Treatment of concurrent infection appropriately if present is advised to prevent a recurrence of the cascade.
References
Adair R Gosmanov, M.D., Ph.D., F.A.C.E. and Abbas E Kitabchi, M.D., Ph.D., M.A.C.E. 2018 Diabetic Ketoacidosis. NCBI. https://www.ncbi.nlm.nih.gov/books/NBK279146/
Erika F. Brutsaert , MD. 2019. Diabetic Ketoacidosis (DKA). MSD manual https://www.msdmanuals.com/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/diabetic-ketoacidosis-dka
Lindy Kahanovitz, MSc,1,2 Patrick M. Sluss, PhD,3 and Steven J. Russell, MD, PhD2. Type 1 Diabetes – A Clinical Perspective NCBI PMC 2018.
LiangyouRui. 2014. Energy Metabolism in the Liver. NCBI PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050641/
Xueping Zhang, Shanshan Yang, Jinglu Chen, and Zhiguang Su 2018. Unraveling the Regulation of Hepatic. NCBI. GluconeogenesisFrontEndocrinol (Lausanne). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6353800/
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