Page 254 - TNFlipTest

E12 Endocrinology Disorders of Glucose Metabolism Toronto Notes 2019 Acute Complications
Table 13. Acute Complications of Diabetes Mellitus: Hyperglycemic Comatose States
Pathophysiology
Diabetic Ketoacidosis (DKA)
• Usually occurs in Type 1 DM
• Insulin deficiency withcounterregulatory hormones (glucagon,
cortisol, catecholamines, GH)
• Can occur with lack of insulin (non-adherence, inadequate dosage, 1st
presentation) or increased stress (surgery, infection, exercise)
• Unopposed hepatic glucose productionghyperglycemiagosmotic diuresisgdehydration and electrolyte disturbancegNa+ (water
shift to ECF causing pseudohyponatremia)
• Fat mobilizationgFFAgketoacidsgmetabolic acidosis
• Severe hyperglycemia exceeds the renal threshold for glucose and
ketone reabsorptiongglucosuria and ketonuria
• Total body K+ depletion but serum K+ may be normal or elevated, 2o to
shift from ICF to ECF due to lack of insulin,  plasma osmolality • Total body PO43- depletion
• Polyuria, polydipsia, polyphagia with marked fatigue, N/V
• Dehydration (orthostatic changes)
• LOC may be  with ketoacidosis or with high serum osmolality (osm
>330 mmol/L)
• Abdominal pain
• Fruity smelling breath • Kussmaul’s respiration
• BG (typically 11-55 mmol/L,Na+ (2o to hyperglycemiagfor every in BG by 10 mmol/L there is ain Na+ by 3 mmol/L)
• Normal orK+,HCO3–,BUN,Cr, ketonemia,PO43-
•  osmolality
• corrected sodium = current sodium + [0.3 x (current glucose -5)]
• Metabolic acidosis withAG, possible 2o respiratory alkalosis
• If severe vomiting/dehydration there may be a metabolic alkalosis
• +ve for glucose and ketones
• ABCs are first priority
• Monitor degree of ketoacidosis with AG, not BG or serum ketone level • NOTE: Anion gap is the most important endpoint used to monitor
the resolution of the metabolic acidosis
• Rehydration
– 500 mL/h x4 h, then 250 mL/h x4 h NS if mild-moderate deficit,
1-2 L/h NS if severe deficit (shock)
– Switch to 0.45% NaCl once euvolemic (continue NS if corrected
[Na+] is low or rate of fall of plasma osmolality ≥3 mosm/kg/h)
– once BG reaches 14.0 mmol/L add D5W or D10W to maintain BG
of 12-14 mmol/L • Insulin therapy
– critical to resolve acidosis, not hyperglycemia
– do not use with hypokalemia (see below), until serum K+ is
corrected to >3.3 mmol/L
– use only regular insulin (R)
– maintain on 0.1 U/kg/h insulin R infusion
– check serum glucose hourly
• K+ replacement
– with insulin administration, hypokalemia may develop
– if serum K+<3.3 mmol/L, give 40 mEq/L K+ replacement and hold
insulin until [K+] ≥3.3mmol/L
– when K+ 3.3-5.0 mmol/L add KCl 10-40 mEq/L to keep K+ in the
range of 3.5-5 mEq/L • HCO3–
– if pH <7.0 or if hypotension, arrhythmia, or coma is present give HCO3– 1 ampoule (50 mmol) in 200 mL D5W (or sterile water if available) over 1 h, repeated q1-2h until pH ≥7.0
– do not give if pH >7.1 (risk of metabolic alkalosis)
– can give in case of life-threatening hyperkalemia
• <1-3.3% mortality in developed countries
• Serious morbidity from sepsis, hypokalemia, respiratory complications,
thromboembolic complications, and cerebral edema (the latter in children)
Hyperosmolar Hyperglycemic State (HHS)
• Occurs in Type 2 DM
• Often precipitated by sepsis, stroke, MI, CHF, renal failure, trauma, drugs
(glucocorticoids, immunosuppressants, phenytoin, diuretics), dialysis, recent
surgery, burns
• Partial or relative insulin deficiency decreases glucose utilization in muscle,
fat, and liver while inducing hyperglucagonemia and hepatic glucose
production
• Presence of a small amount of insulin prevents the development of ketosis
by inhibiting lipolysis
• Characterized by hyperglycemia, hyperosmolality, and dehydration without
ketosis
• More severe dehydration compared to DKA due to more gradual onset and
 duration of metabolic decompensation plus impaired fluid intake which is
common in bedridden or elderly
• Volume contractiongrenal insufficiencyghyperglycemia,osmolality
gshift of fluid from neurons to ECFgmental obtundation and coma • Onset is insidiousgpreceded by weakness, polyuria, polydipsia
• History of decreased fluid intake
• History of ingesting large amounts of glucose containing fluids
• Dehydration (orthostatic changes)
•  LOC g lethargy, confusion, comatose due to high serum osmolality
• Kussmaul’s respiration is absent unless the underlying precipitant has also
caused a metabolic acidosis
• BG (typically 44.4-133.2 mmol/L)
• In mild dehydration, may have hyponatremia (spurious 2o to hyperglycemia g for everyin BG by 10 mmol/L there is ain Na+ by 3 mmol/L)
– if dehydration progresses, may get hypernatremia • Ketosis usually absent or mild if starvation occurs
•  osmolality
• Metabolic acidosis absent unless underlying precipitant leads to acidosis (e.g. lactic acidosis in MI)
• -ve for ketones unless there is starvation ketosis • Glycosuria
• Same resuscitation and emergency measures as DKA • Rehydration
– 500 mL/h x4 h, then 250 mL/h x4 h NS if mild-moderate deficit, 1-2 L/h NS if severe deficit (shock)
– Switch to 0.45% NaCl once euvolemic (continue NS if corrected [Na+] is low or rate of fall of plasma osmolality ≥3 mosm/kg/h)
– once BG reaches 14.0 mmol/L add D5Wor D10W to maintain BG of 12-14 mmol/L
• K+ replacement
– less severe K+ depletion compared to DKA
– if serum K+ <3.3 mmol/L, give 40 mEq/L K+ replacement and hold
insulin until [K+] ≥3.3mmol/L
– when K+ 3.3-5.0 mmol/L add KCL 10-40 mEq/L to keep K+ in the range
of 3.5-5 mEq/L
– if serum K+ ≥5.5 mmol/L, check K+ every 2 h
• Search for precipitating event • Insulin therapy
– Achieved by monitoring plasma osmolality, adding glucose to infusions once BG reaches 14 mmol/L, using correct concentration of saline
– Switch to 0.45% NaCl once euvolemic as urinary loss of electrolytes in osmotic diuresis are usually hypotonic
– Increase saline concentration if falling too rapidly
• Mortality rates between 12-17%, but studies looking at this included mixed DKA/HHS state
Clinical Features
Serum
ABG Urine Treatment
Prognosis