Presentation on theme: " Lack of insulin production prevents glucose uptake by muscle and allows unrestrained hepatic glucose production. Lack of suppression of lipolysis."— Presentation transcript:
Lack of insulin production prevents glucose uptake by muscle and allows unrestrained hepatic glucose production. Lack of suppression of lipolysis leads to excess circulating FFAs which are converted into ketoacids (B-OH-butyrate and acetoacetate) by the liver.
This leads to acidemia which may impair vascular tone and cardiac function. Marked hyperglycemia and ketonemia cause osmotic diuresis with loss of water and electrolytes.
Nausea, emesis Abdominal pain (2/2 delayed gastric emptying/ileus 2/2 acidosis and lyte abnormalities and may correlate with degree of acidosis) Polyuria/Polydipsia Lethargy Headache Anorexia Usually develop over 24h or less in DKA; over multiple days more insidiously in HHS.
B-OH-Butyrate Acetone & Acetoacetate Direct measurement of B-OH-Butyrate is preferable for monitoring degree of ketonemia and is available at UHCMC (not VA) Standard ketones may become increasingly positive as conversion from B- OH-Butyrate to acetone/acetoacetate occurs
5 Step Approach to ABGs without memorizing formulas….
1. Identify alkalosis/acidosis by pH change from 7.4. (>7.4 = alkalosis. <7.4 = acidosis). 2. Determine if primary disorder is respiratory or metabolic based on direction of change of PCO2. If pH and PCO2 change in same direction - metabolic If pH and PCO2 change in opposite direction - respiratory
3. Check compensation to identify other primary disorders. Metabolic Acidosis - Check Resp Compensation. PCO2 = (1.5 × [HCO3-]) + 8 ± 2 Simplified: For every 1 mEq decrease in HCO3, PCO2 should decrease by 1.2 mmHg. Example: If HCO3 is 9...24-9 = 15. PCO2 reduction should be 15x1.2 = 18. 40-18 = 22mmHg. Metabolic Alkalosis – Check Resp Compensation. PCO2 rises 0.7mmHg for each 1.0 mEq rise in HCO3. Example: If HCO3 is 34...34-24 = 10. 10 x 0.7 = 7. 40+7 = 47mmHg.
Acute Respiratory Acidosis: Every 10 mmHg rise in PCO2 = 1 meq rise in HCO3 Chronic Respiratory Acidosis: For every 10 mmHg rise in PCO2 = 3.5 mEq rise in HCO3
Acute Respiratory Alkalosis: Every 10 mmHg drop in PCO2 = 2 meq drop in HCO3 Chronic Respiratory Alkalosis: For every 10 mmHg drop in PCO2 = 5 mEq drop in HCO3
4. If metabolic acidosis - calculate anion gap. Na - (Cl+HCO3) Normal gap 12 or less. For each gram of albumin drop less than 4 add 2.5 to calculated gap to get actual gap. Example: Calculated gap 9. Albumin 2. Add 5 to gap = 14.
5. If AGMA - calculate delta gap. Change in gap divided by change in bicarbonate. (AG-12) / (24-HCO3) <1 – AGMA + NAGMA 1-2 - Pure AGMA >2 – AGMA + Metabolic Alkalosis
In DKA, initially AGMA; as treatment proceeds many will develop a subsequent NAGMA. › Ketoacid anions are excreted in the urine with sodium which would have been used to reproduce HCO3 in the kidney loss of “potential HCO3” which is equivalent to actual bicarb loss subsequent NAGMA.
Q1H POCT Glucose until stable RFP/Serum osmolality q2-4h with close FU of HCO3. Consider VBG rather than frequent ABGs for pt and intern comfort – venous pH is about 0.03 units lower than ABG.
Severe Hypovolemia – NS 1000cc/h Milder Dehydration – evaluate corrected Na (Corrected Na = Measured Na (Glc- 100/100) › Hyponatremia – 250-500cc/h NS › Normal-Hypernatremia – 250-500c/h 1/2NS When serum glc reaches 200 (or 300 in HHS) Change to D51/2NS 150- 250cc/h
Usually IV route except in mild DKA. IV: Regular insulin 0.1U/kg bolus then 0.1U/kg/h continuous infusion OR no bolus with infusion rate alone at 0.14U/kg/h SQ: Lispro 0.3U/kg x1 then 0.2U/kg in 1hr then 0.2U/kg SQ q2h. If serum glc doesn’t fall by 50-70 mg/dL in 1 st hour double the IV or SQ dose. K <3.3 is a CONTRAINDICATION to insulin.
When glc to 200 (in DKA) or 250-300 (in HHS) reduce infusion to 0.02-0.05U/kg/h IV or change SQ dosing to 0.1U/kg q2h with goal glc 150-200. Never discontinue insulin prior to closure of anion gap!
If K <3.3 – hold insulin therapy and replete K with fluids – 40-60mEq/h to ½NS until K 3.3+ (assuming UOP 50cc/h+). If K >5.3 – no K supplementation but check q2h. 3.3-5.3 – Give 20-30mEq per liter of 1/2NS goal K 4-5 (assuming UOP 50cc/h+). Substantial losses in almost all 2/2 urine loss; shifts out of cells 2/2 insulin deficiency and hyperosmolality so K artifically elevated at presentation.
Whole body PO4 depletion is common though PO4 will be normal or elevated initially due to migration out of cells. With treatment hypophosphatemia will develop usually without adverse effects in a self-ltd fashion. No benefit to repleting PO4 unless cardiac dysfx/hemolytic anemia/resp depression, concentration <1.
pH <6.9 Consider HCO3 gtt (though small studies have shown minimal benefit…) pH >7.0 No HCO3
Ketoacidosis resolved – AG is normal (<12) › Ketonemia/Ketonuria may persist >36h without pt actually being in true ketoacidosis. HHS pts are mentally alert and plasma osmolality is <315. Pt is able to tolerate PO.
Initiate SQ insulin AT MEALTIME with a 1- 2h taper of the gtt. Insulin Naïve 0.5-0.8U/kg per day in sliding scale + long-acting regimen › 25% as long acting. › 25% as scheduled meal-time insulin › Sliding Scale Known DM start at previous insulin regimen.
Cerebral edema › Very rare in adults but 40% mortality. › Sxs: ha, lethargy, decreased arousal seizures, incontinence, brady, resp arrest, pupul changes. › Mortality 20-40%. Prevented by following protocol, adding dextrose to fluids when appropriate. Tx – unit, mannitol?, 3%NS?
Non-cardiogenic pulmonary edema › Hypoxemia 2/2 decreased osmotic pressure migration of fluid into lungs. › If initial A-a gradient is widened on ABG, higher risk of development of pulmonary edema.
A 23-year-old woman with type 1 diabetes mellitus is admitted to the hospital with a diagnosis of community-acquired pneumonia and lethargy. Before admission, her insulin pump therapy was discontinued because of confused mentation. On physical examination, temperature is 37.5 °C (99.5 °F), blood pressure is 108/70 mm Hg, pulse rate is 100/min, and respiration rate is 24 min. There are decreased breath sounds in the posterior right lower lung. Neurologic examination reveals altered consciousness.
Which of the following is the most appropriate next step in management? AAdd insulin glargine BAdd neutral protamine Hagedorn (NPH) insulin CImplement a sliding scale for regular insulin DStart an insulin drip