ETOSIS DISORDERS

by Nick Mark MD ONE

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ETIOLOGY OF KETOSIS version →
Ketone bodies are a normal metabolic energy source. Excessive unregulated production of @nickmmark
ketones, often accompanied by an anion gap acidosis, is seen in several disease states: Starvation Euglycemic DKA/HHS
AKA DKA HHS
Ketosis DKA Overlap
· Starvation ketosis – normal consequence of fatty acid (FA) metabolism. Tx: provide
carbohydrates (IVF or PO): The pt will produce endogenous insulin normally. Treat Physiologic Seen in Seen w/ SGLT2 DM1 (or ketosis DM1/2 DM2
other deficiencies (thiamine). Monitor for development of re-feeding syndrome. Etiology switch to FA chronic inhibitors, prone DM2) Highest mo
metabolism. alcoholics pregnancy Young > elderly rtality Elderly > young
· Alcoholic ketoacidosis (AKA) – seen in chronic alcoholics, often can be treated
with dextrose containing IVF & thiamine. Treat concomitant alcohol withdrawal.
· Diabetic ketoacidosis (DKA) – caused by complete insulin deficiency, leading to 800-
BG (mg/dL) <250 <250 <250 400-800 >800-1200
1000
marked anion gap acidosis (pH < 7.35) w/ elevated blood glucose. Euglycemic DKA is
a variant seen with SGLT inhibitors & pregnancy, where blood glucose (BG) is normal. Ketones ++++ ++ +++ +++ + -
· Hypeglycemic hyposmolar state (HHS) –partial insulin deficiency, causing minimal
ketosis but marked increase in BG & osmolality. Glucosuria causes massive volume loss. Acidosis - ++ +++ +++ ++ +
· DKA/HHS Overlap – features of both DKA & HHS and treated the same.
Fluid deficit (L) - - 2-4 L 6-8 L 6-10 LWhen BG 8-10 L
CAUSES/WORKUP OF DKA/HHS INSULIN bolus & gtt When AG
Identifying the cause of DKA/HHS is essential, because missing the underlying WHICH KETONE TO CHECK?
normal, add closed give
glucose to IVF SQ INSULIN
etiology is responsible for much of the morbidity/mortality. Consider the 5 I’s: Checking BHB is more accurate (fewer false positives & false negatives)

BG, AG, & Fluid Deficit

Etiology Workup Nitroprusside urine test is unreliable.
Infection BCx, Ucx, Procalcitonin, CXR, exam, POCUS Fatty acid (FA) IVF boluses for
breakdown hypovolemic
Ischemia Lactate, Troponin, EKG shock
β-hydroxybutyrate Acetoacetate Acetone NORMAL RANGE
Inflammation Lipase, CRP Gradual correction of
remaining fluid deficit
Blood test Urine test Breath test or
Intoxication Serum Osmolarity (Osm), Blood EtOH, Utox
(most accurate) (semi-quantitative) “sweat” breath odor INITIAL INTERMEDIATE RESOLUTION
Insulin (deficiency) History (e.g. ran out of insulin, oral meds)
Phase
Consider new meds (e.g. steroids, diuretics, etc) INITIAL PHASE INTERMEDIATE PHASE RESOLUTION PHASE
Resuscitation & stabilization Gradual correction Normalization & de-escalation
TREATMENT OF KETOSIS: INSULIN Bolus INSULIN 10 units IV then Adjust INSULIN gtt to achieve
Once AG closed, give SQ
The three pillars of treating DKA/HHS are INSULIN GOAL: correct BG, AG, & acidosis INSULIN. 0.1 units/kg. Stop
Start INSULIN gtt 0.1 units/kg/hr 50 mg/dL/hr reduction in BG INSULIN gtt 2 hrs later
(to stop ketogenesis), IVF (to restore fluid deficit & Monitor BG, Chem10
correct hyperosmolarity), & ELECTROLYTES (to
(Don’t add K to IVF as it
correct numerous derangements & prevent arrythmia) slows rate of infusion)
HHS requires more FLUID and less INSULIN than DKA Replete K+ to >4 mEq/L Use caution if K+ < 3.3 mmol/L; Resume diet; Start
ELECTROLYTES
(because of greater fluid deficit and less acidosis) (ideally both PO and IV) consider decreasing insulin gtt basal, prandial, &
GOAL: normalize K+, Mg2+, Ca2+, PO4, correction INSULIN.
Mild DKA can be treated with SQ INSULIN in the ED and HCO3 to avoid arrythmias If HCO3 < 6.9 give Correct Mg deficits to
Stop IVF. Begin oral
or medical wards (does not require ICU admission) Monitor Chem10, ± VBG, EKG NaHCO3 bolus ± gtt reduce further K wasting
ELECTROLYTE

v1.1 (2022-06-14) CC BY-SA 3.0

(Acidosis greatly increases the risk replacement.
Expected AG is 2.5x albumin (usually <12 mOsm/L); of cardiac arrest during intubation;
with treatment AG should normalize to expected consider NIPPV)
Replace fluid deficits with
AG. If not improving consider concomitant IV FLUID isotonic IVF ~200 ml/hr Once
GOAL: restore circulating volume, tolerating PO
lactic acidosis or other metabolic derangement. If in hypovolemic shock,
correct fluid deficit & hyperosmolarity, correct rapidly w/ IVF boluses Once corrected Na is >140
Corrected Sodium accounts for spurious low Na+ avoid cerebral edema by correcting the mEq/L switch to hypotonic IVF When BG < 200 mg/dL switch
(e.g. 1 L of LR or 0.9% NS)
measurements when blood glucose is high. For corrected sodium gradually. to avoid overcorrection to glucose containing IVF
every 100 mg/dL increase in BG, the corrected Na (Use volume responsiveness to guide (e.g. D5LR or D5 ½NS)
calculate corrected Na & Fluid Deficit (e.g. 0.45% NS, LR)
resuscitation; Consider balanced
is increased by 2.4 mEq/L. Monitor Osm, serum Na, urine output crystalloids. E.g Plasmalyte 148)