Diabetic Ketoacidosis (dka)
Diabetic ketoacidosis is a condition that results from when the body is deprived of the ability to use glucose as an energy source. Usually this is due to a lack of insulin. Insulin is used to uptake glucose into the cells to be used for energy. If there is no insulin or the cells are resistant to insulin, the blood sugar levels increase to dangerous levels for the patient. It seems counter intuitive that the patient wouldn't have energy with such high levels of glucose, but this glucose is essentially unusable without insulin. Because your body needs energy to survive, it starts turning to alternative fuel sources (fat). Fat cells start breaking down and, as a result, release ketones (which are acidic) into the bloodstream. Hence the name: diabetic ketoacidosis. “High levels of ketones can poison the body. When levels get too high, you can develop DKA. DKA may happen to anyone with diabetes, though it is rare in people with type 2. Treatment for DKA usually takes place in the hospital. But you can help prevent it by learning the warning signs and checking your urine and blood regularly.” Causes The most common causes of DKA are not getting enough insulin, having a severe infection, becoming dehydrated, or a combination of these issues. It seems like it occurs mainly in patients with type one diabetes. Symptoms Some of the symptoms that people experience with DKA include the following: Excessive thirst and urination (more water is pulled into the urine as a result of high ketone loss in the urine) Lethargy Breathing very quickly (patients have a very high level of acids in their bloodstream and they try to "blow" off carbon dioxide by breathing quickly) A fruity odor on their breath (ketones have a fruity smell) Nausea and vomiting (the body tries to get rid of acid Continue reading >>
Osmolality Gap - Calculation And Interpretation
Osmolality Gap - Calculation and Interpretation Plasma osmolality is determined mainly by Sodium (NA), its counter ions, and uncharged species such as Glucose (GLU) and Urea (UN). Knowledge of the plasma concentration of these species allows calculation of the plasma osmolality quite accurately. The difference between measured osmolality (MO) and calculated osmolality (CO) is known as the osmolar gap (OG). A large positive (>15) osmolar gap can help identify the presence in plasma of substances such as ethanol, methanol, isopropanol, ethylene glycol, propylene glycol (found as a diluent for some intravenous medications such as lorazepam), and acetone. The formula given below was instituted at the University of Iowa Hospitals and Clinics for use on plasma samples starting November 2009 and is based on a published study comparing different calculated osmolality formulas (see ref. 3): (1). CO = 2 x NA + 1.15 * GLU/18 + BUN/2.8 : calculated osmolality To calculate the osmolar gap, plasma determination of MO, NA, GLU, and BUN are necessary. Proper interpretation of the OG also requires knowledge of the anion gap (AG = NA - HCO3 - CL), the blood pH, and qualitative testing of the plasma ketone bodies (KETO). Determinations of MO and for CO should be performed on the same plasma sample. An OG value greater than 15 has traditionally been considered a critical value or cutoff. Approximately 97% of osmolar gaps in patients are between -10 and +10. When the OG is combined with blood pH and AG, poisonings with toxic alcohols can be quickly recognized. The presence of low blood pH, elevated AG, and greatly elevated OG (>15) is a medical emergency that requires prompt treatment. The specific agent(s) responsible can be identified by the gas chromatographic assays for ethanol, methan Continue reading >>
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Metabolic Acidosis; Non-gap
Pseudoaldosteronism, type 2 (Gordons syndrome) B. Describe a diagnostic approach/method to the patient with this problem. Metabolic acidosis can be divided into two groups based on anion gap. If an anion gap is elevated (usually greater than 12), see gapped metabolic acidosis. Diagnosis of the cause of non-gapped metabolic acidosis is usually clinically evident as it can be attributed to diarrhea, intravenous saline or by default, renal tubular acidosis. Occasionally, it may not be clear whether loss of base occurs due to the kidney or bowel. In such a case, one should calculate the urinary anion gap. The urinary anion gap (UAG) = sodium (Na+)+K+ chloride (Cl). Caution if ketonuria or drug anions are in the urine as it would invalidate the calculation. Renal tubular acidosis: UAG is positive value. As an aid, UAG is neGUTive when associated with bowel causes. Non-gapped metabolic acidosis can further be divided into two categories: 1. Historical information important in the diagnosis of this problem. The urinary anion gap is key to determining if the non-gapped metabolic acidosis is GI or renal. The urinary anion gap provides an estimate of the urinary ammonium (NH4+) excretion. The urinary anion gap is defined as UAG = Unmeasured Anion (UA) Unmeasured Cation (UC). As seen in diarrhea, bicarbonate is excreted via the gut triggering urinary ammonium excretion to maintain electroneutrality. This causes an increased UC (urinary NH4+) and results in a negative UAG. On the other hand, renal tubular acidosis involve the inability of the kidney to resorb bicarbonate. This causes an increased UA (urinary HCO3) and results in a positive UAG. It is worthy to understand how the urinary anion gap was derived. The cations present in urine include: Na+, K+, Ca2+, Mg. The anions in u Continue reading >>
Metabolic Acidosis Nursing Management And Interventions - Nurseslabs
Metabolic Acidosisis an acid-base imbalance resulting from excessive absorption or retention of acid or excessive excretion of bicarbonate produced by an underlying pathologic disorder. Symptoms result from the bodys attempts to correct the acidotic condition through compensatory mechanisms in the lungs , kidneys and cells. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium . High anion gap acidosis occurs in diabetic ketoacidosis ; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl. Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/ diarrhea , small-bowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride). This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit. Use of carbonic anhydrase inhibitors or anion-exchan Continue reading >>
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Diabetic Ketoacidosis In Pregnancy
Diagnosis of DKA: � Initial STAT labs include • CBC with diff • Serum electrolytes • BUN • Creatinine • Glucose • Arterial blood gases • Bicarbonate • Urinalysis • Lactate • Serum ketones • Calculation of the Anion Gap � serum anion gap = serum sodium – (serum chloride + bicarbonate) • Electrocardiogram Treatment Protocol for Diabetic Ketoacidosis Reviewed 5/2/2017 2 Updated 05/02/17 DKA Diagnostic Criteria: � Blood glucose >250 mg/dl � Arterial pH <7.3 � Bicarbonate ≤18 mEq/l � Anion Gap Acidosis � Moderate ketonuria or ketonemia 1. Start IV fluids (1 L of 0.9% NaCl per hr initially) 2. If serum K+ is <3.3 mEq/L hold insulin � Give 40 mEq/h until K ≥ 3.3 mEq/L 3. Initiate DKA Order Set Phase I (*In PREGNANCY utilize OB DKA order set) 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) RN will titrate per DKA protocol Insulin Potassium Bicarbonate IVF Look for the Cause - Infection/Inflammation (PNA, UTI, pancreatitis, cholecystitis) - Ischemia/Infarction (myocardial, cerebral, gut) - Intoxication (EtOH, drugs) - Iatrogenic (drugs, lack of insulin) - Insulin deficiency - Pregnancy DKA/HHS Pathway Phase 1 (Adult) Approved by Diabetes Steering Committee, MMC, 2015, Revised DKA Workgroup 1_2016 Initiate and continue insulin gtt until serum glucose reaches 250 mg/dl. RN will titrate per protocol to achieve target. When sugar < 250 mg/dl proceed to DKA Phase II *In PREGNANCY when sugar <200 proceed to OB DKA Phase II *PREGNANCY � Utilize OB DKA order set Phase 1 � When glucose reaches 200mg/dL, Initiate OB DKA Phase 2 � Glucose goals 100-150mg/dL OB DKA Phase 2 Determine hydration status Hypovolemic shock Mild hypotensio Continue reading >>
Can Serum Β-hydroxybutyrate Be Used To Diagnose Diabetic Ketoacidosis?
Abstract OBJECTIVE—Current criteria for the diagnosis of diabetic ketoacidosis (DKA) are limited by their nonspecificity (serum bicarbonate [HCO3] and pH) and qualitative nature (the presence of ketonemia/ketonuria). The present study was undertaken to determine whether quantitative measurement of a ketone body anion could be used to diagnose DKA. RESEARCH DESIGN AND METHODS—A retrospective review of records from hospitalized diabetic patients was undertaken to determine the concentration of serum β-hydroxybutyrate (βOHB) that corresponds to a HCO3 level of 18 mEq/l, the threshold value for diagnosis in recently published consensus criteria. Simultaneous admission βOHB and HCO3 values were recorded from 466 encounters, 129 in children and 337 in adults. RESULTS—A HCO3 level of 18 mEq/l corresponded with βOHB levels of 3.0 and 3.8 mmol/l in children and adults, respectively. With the use of these threshold βOHB values to define DKA, there was substantial discordance (∼≥20%) between βOHB and conventional diagnostic criteria using HCO3, pH, and glucose. In patients with DKA, there was no correlation between HCO3 and glucose levels on admission and a significant but weak correlation between βOHB and glucose levels (P < 0.001). CONCLUSIONS—Where available, serum βOHB levels ≥3.0 and ≥3.8 mmol/l in children and adults, respectively, in the presence of uncontrolled diabetes can be used to diagnose DKA and may be superior to the serum HCO3 level for that purpose. The marked variability in the relationship between βOHB and HCO3 is probably due to the presence of other acid-base disturbances, especially hyperchloremic, nonanion gap acidosis. Recently published consensus criteria for diagnosing diabetic ketoacidosis (DKA) include a serum bicarbonate (HCO3) Continue reading >>
Abg Interpretation
Arterial blood gas (ABG) interpretation is something many medical students find difficult to grasp (we’ve been there). We’ve created this guide, which aims to provide a structured approach to ABG interpretation whilst also increasing your understanding of each results relevance. The real value of an ABG comes from its ability to provide a near immediate reflection of the physiology of your patient, allowing you to recognise and treat pathology more rapidly. To see how to perform an arterial blood gas check out our guide here. If you want to put your ABG interpretation skills to the test, check out our ABG quiz here. Normal ranges pH: 7.35 – 7.45 PaCO2: 4.7-6.0 kPa PaO2: 11-13 kPa HCO3-: 22-26 mEg/L Base excess: -2 to +2 mmol/L Patient’s clinical condition Before getting stuck into the details of the analysis, it’s important to look at the patient’s current clinical status, as this provides essential context to the ABG result. Below are a few examples to demonstrate how important context is when interpreting an ABG. A normal PaO2 in a patient on high flow oxygen – this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy A normal PaCO2 in a hypoxic asthmatic patient – a sign they are tiring and need ITU intervention A very low PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations – likely a venous sample Oxygenation (PaO2) Your first question when looking at the ABG should be “Is this patient hypoxic?” (because this will kill them long before anything else does). PaO2 should be >10 kPa on air in a healthy patient If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa less than the % inspired concentration / FiO Continue reading >>
Anion Gap (blood) - Health Encyclopedia - University Of Rochester Medical Center
If you may have swallowed a poison, such as wood alcohol, salicylate (in aspirin), and ethylene glycol (in antifreeze), your provider may test your blood for it. If your provider thinks you have ketoacidosis, you might need a urine dipstick test for ketone compounds. Ketoacidosis is a health emergency. Many things may affect your lab test results. These include the method each lab uses to do the test. Even if your test results are different from the normal value, you may not have a problem. To learn what the results mean for you, talk with your healthcare provider. Results are given in milliequivalents per liter (mEq/L). Normal results are 3 to 10mEq/L, although the normal level may vary from lab to lab. If your results are higher, it may mean that you have metabolic acidosis. Hypoalbuminemia means you haveless albumin protein than normal. If you have this condition, your expected normal result must be lower. The test requires a blood sample, which is drawn through a needle from a vein in your arm. Taking a blood sample with a needle carries risks that include bleeding, infection, bruising, or feeling dizzy. When the needle pricks your arm, you may feel a slight stinging sensation or pain. Afterward, the site may be slightly sore. Being dehydrated or retaining water in your body can affect your results. Antibiotics such as penicillin can also affect your results. You don't need to prepare for this test. But be sure your healthcare provider knows about all medicines, herbs, vitamins, and supplements you are taking. This includes medicines that don't need a prescription and any illicit drugs you may use. Continue reading >>
Severe Ketoacidosis Associated With Canagliflozin (invokana): A Safety Concern
Case Reports in Critical Care Volume 2016 (2016), Article ID 1656182, 3 pages 1Section of Pulmonary and Critical Care Medicine, Providence Hospital and Medical Center, 16001 W 9 Mile Road, Southfield, MI 48075, USA 2Department of Internal Medicine, Providence Hospital and Medical Center, 16001 W 9 Mile Road, Southfield, MI 48075, USA Academic Editor: Kurt Lenz Copyright © 2016 Alehegn Gelaye et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Canagliflozin (Invokana) is a selective sodium glucose cotransporter-2 (SGLT-2) inhibitor that was first introduced in 2013 for the treatment of type 2 diabetes mellitus (DM). Though not FDA approved yet, its use in type 1 DM has been justified by the fact that its mechanism of action is independent of insulin secretion or action. However, some serious side effects, including severe anion gap metabolic acidosis and euglycemic diabetic ketoacidosis (DKA), have been reported. Prompt identification of the causal association and initiation of appropriate therapy should be instituted for this life threatening condition. 1. Introduction More than 5 million patients are admitted annually to intensive care units (ICUs) in the United States. A number of life threatening medical conditions, including diabetic ketoacidosis, can be associated with metabolic acidosis. Metabolic acidosis may also arise from several drugs and toxins through a variety of mechanisms. Since approval of the first-in-class drug in 2013, data have emerged suggesting that Sodium Glucose Transporter-2 (SGLT-2) inhibitors, including canagliflozin, may lead to diabetic ketoacidosis [1]. We pre Continue reading >>
Serum Anion Gap | Usmle Pearls
Formula: SAG = (Na+ + K+) (Cl + HCO3) When Used? To differentiate between the causes of Metabolic Acidosis. Interpretation: If SAG is >12 then the metabolic acidosis is Increased Anion Gap Metabolic Acidosis. Remember the mnemonic MUDPILES for Increased Anion Gap Metabolic Acidosis: Methanol, Uremia, DKA, Propylene Glycol, Iron Poisoning/Isoniazid, Lactic Acidosis, Ethylene Glycol, Salicylates. Formula: OG = Measured Serum Osmolality Calculated Serum Osmolality When Used? To diagnose poisoning by certain alcohols. Interpretation: If >10, consider Ethanol, Methanol, Ethylene Glycol, Isopropyl Alcohol and Propylene Glycol Intoxication. (Remember Isopropyl Alcohol has Increased OG but not Increased SAG! (i.e. doesnt cause AG Metabolic Acidosis)) When Used? To differentiate between causes of Normal AG Metabolic Acidosis i.e. to differentiate between RTA vs Diarrhea as cause of the Normal AG Metabolic Acidosis Interpretation: Remember by (Na+ + K+ Cl) we are actually measuring (Urine Cations Urine Anions), the major Cation in Urine that is not usually measured is NH4+, so if UAG is negative that means Increased NH4+ (i.e. acid) excretion in the Urine which should be the case in any acidosis INCLUDING Diarrhea! But, if renal function is not normal as in RTA, NH4+ is not excreted in Urine and so UAG will be 0 or Positive. So, in Normal Anion Gap Metabolic Acidosis, if: UAG = Negative value > Diarrhea (Remember NeGUTive) Formula: Stool Osmolality (usually not measured and replaced by 290 for ease of calculation) 2 (stool Na+ + stool K+) When Used? To differentiate Secretory vs Osmotic Diarrhea SOG >100 = Osmotic Diarrhea (e.g. Lactose Intolerance) Continue reading >>
Metabolic Acidosis
Increases 0.3-0.7 mEq/l [0.3-0.7 mmol/L] per 0.1 decr pH Difference between measured plasma cation (ie, Na+) and anions (ie, chloride (Cl-), HCO3-) concentrations Lactic acidosis (mild LA may have normal AG) Also called hyperchloremic acidosis (decreased HCO3, increased Cl) Renal tubular acidosis: impairment in renal acidification Type III (term no longer used) Formerly used to define distal RTA with bicarbonate wasting in children Bicarbonaturia resolves with age and is not truly part of a pathologic process Type IV: common in obstructive nephropathy, DM, hyporenin/hypoaldosteronehyper K+, acidosis Intestinal loss of bicarbonate (diarrhea, pancreatic fistula) Carbonic anhydrase inhibitors (e.g. acetazolamide) Dilutional acidosis (due to rapid infusion of bicarbonate-free isotonic saline) Ingestion of exogenous acids (ammonium chloride, methionine, cystine, calcium chloride) Drugs: amiloride, triamterine, Bactrim, chemotherapy, pentamidines As diagnostic aid, is not absolute "Delta gap" = calculated anion gap:nl anion gap In anion gap acidosis, "delta gap" should equal "delta HCO3" If HCO3 higher than predictedsuperimposed metabolic alkalosis If HCO3 lower than predictedsuperimposed non-anion gap metabolic acidosis Allows diagnosisof mixed metabolic disturbance Mixed metabolic disturbance plus respiratory disturbance Check urine pH before initializing therapy NaHCO3 therapy for pH < 7.1 - 7.2 Only used emergently to raise pH to > 7.1 or 7.2 Controversial, depends on disorder and symptoms i.e. NaHCO3 not beneficial in DKA treatment with pH under 7.0) DO NOT give this entire amount 2 ampulesof 8.4% NaHCO3 in 1 Liter of 1/4 NS OR 3-4 ampulesof 8.4% NaHCO3 in 1 Liter D5W Overaggressive NaHCO3"overshoot alkalosis" Bicarbonate level should be corrected only to 15 mEq/L [15 m Continue reading >>
Serum Anion Gap: Its Uses And Limitations In Clinical Medicine
Abstract The serum anion gap, calculated from the electrolytes measured in the chemical laboratory, is defined as the sum of serum chloride and bicarbonate concentrations subtracted from the serum sodium concentration. This entity is used in the detection and analysis of acid-base disorders, assessment of quality control in the chemical laboratory, and detection of such disorders as multiple myeloma, bromide intoxication, and lithium intoxication. The normal value can vary widely, reflecting both differences in the methods that are used to measure its constituents and substantial interindividual variability. Low values most commonly indicate laboratory error or hypoalbuminemia but can denote the presence of a paraproteinemia or intoxication with lithium, bromide, or iodide. Elevated values most commonly indicate metabolic acidosis but can reflect laboratory error, metabolic alkalosis, hyperphosphatemia, or paraproteinemia. Metabolic acidosis can be divided into high anion and normal anion gap varieties, which can be present alone or concurrently. A presumed 1:1 stoichiometry between change in the serum anion gap (ΔAG) and change in the serum bicarbonate concentration (ΔHCO3−) has been used to uncover the concurrence of mixed metabolic acid-base disorders in patients with high anion gap acidosis. However, recent studies indicate variability in the ΔAG/ΔHCO3− in this disorder. This observation undercuts the ability to use this ratio alone to detect complex acid-base disorders, thus emphasizing the need to consider additional information to obtain the appropriate diagnosis. Despite these caveats, calculation of the serum anion gap remains an inexpensive and effective tool that aids detection of various acid-base disorders, hematologic malignancies, and intoxication Continue reading >>
Arterial Blood Gases (blood Gases), Acidosis And Alkalosis
Sample The better choice is the Radial artery. The sample may be taken from the femoral artery or brachial. The tests are done immediately because oxygen and carbon dioxide are unstable. Arterial blood is better than the venous blood. For arterial blood don't use the tourniquet and no pull on the syringe plunger. For venous blood syringe or tubes are completely filled and apply a tourniquet for few seconds. Arterial VS Venous blood Arterial blood gives good mixture of blood from various areas of the body. Venous blood gives information of the local area from where the blood sample is taken. Metabolism of the extremity varies from area to area. Arterial blood measurement gives the better status of the lung oxygenating the blood. Arterial blood gives information about the ability of the lung to regulate the acid-base balance through retention or release of CO2. Precautions for the collection of blood Avoid pain and anxiety to the patient which will lead to hyperventilation. Hyperventilation due to any cause leads to decreased CO2 and increased pH. Keep blood cool during transit. Don't clench finger or fist. This will leads to lower CO2 and increased acid metabolites. pCO2 values are lower in the sitting or standing position in comparison with the supine position. Don't delay the performance of the test. Avoid air bubbles in the syringe. Excess of heparin decreases the pCO2 may be 40% less. Not proper mixing of the blood before running the test. Purpose of the test This test is done on the mostly hospitalized patient. Mostly the patients are on ventilator or unconscious. For patients in pulmonary distress. To assess the metabolic (renal) acid-base and electrolytes imbalance. Its primary use is to monitor arterial blood gases and pH of blood. Also used to monitor oxygenatio Continue reading >>
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Serum Anion Gap | Md Nexus
Clinical Utility: calculation of the anion gap is useful to differentiate anion gap metabolic acidoses (AGMA) (see Metabolic Acidosis-Elevated Anion Gap , [[Metabolic Acidosis-Elevated Anion Gap]]) from non-anion gap metabolic acidoses (NAGMA) (see Metabolic Acidosis-Normal Anion Gap , [[Metabolic Acidosis-Normal Anion Gap]]) Anion gap reflects the difference between unmeasured anions (i.e. the anions in the blood that are not routinely measured) unmeasured cations Normal Anion Gap Values: laboratory-dependent (so the laboratory should publish their normal range) Correction of Anion Gap for Serum Albumin: since albumin represents the major unmeasured anion responsible for the anion gap (with a net negative charge at physiologic pH), the expected anion gap must be corrected for serum albumin Anion Gap Decreases 2.3-2.5 mEq/L for Each 1 g/dL Decrease in the Serum Albumin: Corrected Anion Gap = (Measured Anion Gap) + [2.5 x (4.5 Serum Albumin)] Correction of Anion Gap for Hyperkalemia: since potassium is an unmeasured cation For example, serum potassium of 6.0 mEq/L will decrease the anion gap by 2 mEq/L Correction of Anion Gap for Hypercalcemia: since calcium is an unmeasured cation, hypercalcemia decreases the anion gap Correction of Anion Gap for Hypermagnesemia: since magnesium is an unmeasured cation, hypermagnesemia decreases the anion gap Comparison of the Delta Gap and Delta Bicarbonate In an Isolated Anion Gap Metabolic Acidosis, the Delta Gap = Delta Bicarbonate: anion gap generally increases by the same amount that the serum bicarbonate decreases (however, there are exceptions, as noted below) Delta Anion Gap/Delta Bicarbonate Ratio in Lactic Acidosis is Typically Around 1.6: although since hydrogen ion buffering in cells and bone may take several hours to equi Continue reading >>
Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State
Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>
