This document discusses glucose homeostasis and the management of hyperglycemic and hypoglycemic emergencies by emergency physicians. It covers diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), providing diagnostic criteria and pathophysiology. Treatment priorities for DKA include fluid resuscitation followed by insulin and electrolyte replacement. Complications of DKA and HHS as well as hypoglycemia are also reviewed. Case scenarios demonstrate the appropriate treatment approach for different patients presenting with altered mental status and hyperglycemia.

1. Dr Soumar Dutta
Consultant & Coordinator– Emergency Medicine
Narayana Superspeciality Hospital, Guwahati
LOW TO HIGH SUGARS - WHAT AN ED PHYSICIAN
MUST KNOW

2. Glucose is an obligate metabolic fuel for the tissues under physiologic conditions
INTRODUCTION
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the two most common
hyperglycemic acute complications of diabetes. Its overtreatment – usually with insulin – leads to
hypoglycemia
Both hyperglycemic or hypoglycemic emergencies are associated with immediate and long-term adverse
clinical outcomes and can be fatal if not recognized and treated timely.
60-150
mg/dl
HyperglycemiaHypoglycemia

3. GLUCOSE HOMEOSTASIS
Sources
GI
GlycogenolysisGluconeogenesis
Lactate/Pyruvate
Amino Acids
Glycerol

4. GLUCOSE REGULATORY MECHANISM
Hormonal
Neurohormonal
Autoregulatory
Factor

5. DKA
It is a serious acute metabolic complication of type 1 diabetes and ketosis-prone type 2 diabetes
DKA
Hyperglycemia
KetonemiaMetabolic acidosis
The biochemical diagnostic criteria for DKA are :
•Ketonemia >3.0 mmol/L or significant ketonuria
(more than 2+ on standard urine sticks)
•Blood glucose >11 mmol/L or known diabetes
mellitus
•Bicarbonate (HCO3
−) <15 mmol/L and/or venous
pH < 7.3

6. HHS
It is a life-threatening emergency that, although less common than its counterpart, DKA, has a much
higher mortality rate, reaching up to 5-10%.
HHS was previously termed hyperosmolar hyperglycemic non-ketotic coma (HHNC); however, the
terminology was changed because coma is found in fewer than 20% of patients with HHS
HHS is most commonly seen in patients with type 2 DM who have some concomitant illness that leads to
reduced fluid intake

7. CRITERIA FOR HHS
Plasma glucose level of 600 mg/dL or greater
Effective serum osmolality of 320 mOsm/kg or greater
Profound dehydration, up to an average of 9L loss
Serum pH greater than 7.30
Bicarbonate concentration greater than 15 mEq/L
Small ketonuria and low to absent ketonemia
Some alteration in consciousness

8. PATHOPHYSIOLOGY - DKA & HHS

9. DKA & HHS
Mild Moderate Severe HHS
Plasma Glucose (mg/dl) > 250 > 250 > 250 > 600
Arterial pH 7.25-7.30 7.00-7.24 < 7 > 7.30
Serum bi-carbonate(mEq/L)) 15-18 10-15 < 10 > 15
Urine Ketones Positive Positive Positive Small
Serum Ketones Positive Positive Positive Small
Effective osmolarity Variable Variable Variable > 320
AG > 10 > 12 > 12 < 12
Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma
DKA

10. CAUSES LEADING TO DKA & HHS
Omission or reduced daily insulin injections
Infection
Pregnancy
Hyperthyroidism, pheochromocytoma, Cushing’s syndrome
Substance abuse (cocaine)
Medications: steroids, antipsychotics, sympathomimetics,
thiazides
Heat-related illness
Cerebrovascular accident
GI hemorrhage
Myocardial infarction
Pulmonary embolism
Pancreatitis
Major trauma
Surgery

11. CASE SCENARIO - 01
E. IV Normal Saline
D.IV Potassium
C. IV Phosphates
B. IV Lactated Ringers
A. IV Bicarbonate
A 37-year-old male presents to the ED with altered mental status. He was found unconscious at work. On
examination, he is arousable to painful stimulus. His airway is intact and he has bilateral breath sounds. His
initial vital signs are BP - 95/47, PR - 110, RR - 14, O2 % 97% on room air, Temp- 99.4. He has dry mucus
membranes. Fingerstick glucose is 396 mg/dl. Lab work reveals a normal CBC, 3+ acetone, Na 121, Cl− 97,
HCO3 - 9, K 3.0, Mg 2.9, Phos 1.5, AG 29. Which of the following is the first priority in caring for this patient?

12. E. IV Normal Saline
DKA, it is very important to prioritize therapeutic interventions.
The order of therapeutic priorities is volume resuscitation first and foremost, with the aim of:
• Restore the circulatory (intravascular) volume
• Improve tissue /renal perfusion
• Correct hyperosmolality
• Improves insulin sensitivity by reducing circulatory counterregulatory hormones.
DKA HHS
Water Deficit 100 ml/Kg 100-200ml/Kg
Corrected [Na + ] = 1.6 × glucose (mg/dL) − 100 + [measured Na+]
100
2.4 , BG > 400 mg/dl

13. The goal is to replace half the estimated water deficit over a period of 24 hours
Isotonic saline (0.9% NaCl) at a rate of 500 to 1000 mL/hour during the first 1 to 2 hours is usually
sufficient to restore blood pressure and renal perfusion.
Hemodynamics
State of hydration
Serum electrolyte levels
Urinary output
Once the plasma glucose is ∼250 mg/dL, 5% to 10% dextrose should be added to replacement fluids to
allow continued insulin administration until ketonemia is controlled, while at the same time avoiding
hypoglycemia.
0.45 %250- 500 ml/Hr..9 %

14. TYPICAL DEFICITS IN DKA AND HHS
DKA HHS
Sodium 7-10 mmol/kg 5-13 mmol/kg
Phosphate 1 mmol/kg 3-7 mmol/Kg
Potassium 3-5 mmol/kg 4-6 mmol/kg
Chloride 3-5 mmol/kg 5-15 mmol/kg

15. POTASSIUM DEFICIT AND REPLACEMENT
If initial [K+] >5.2 initiate IV infusion of regular insulin. Repeat
[K+] in 2 hours.
If initial [K+] is >3.3 and <5.2 add 20-30 mEq of [K+]to each
liter of fluid and start insulin drip.
If initial [K+] is < 3.3 hold insulin drip and give [K+] @ 20-30
mEq/h until [K+] is >3.3 then initiate insulin.
Despite total body [K+] deficit there is spurious normal ~ high measured [K+] values
Cells
K
+
K
+
Acidemia
Insulin Deficiency
Hypertonicity

16. BICARBONATE REPLACEMENT
HCO3 is not routinely recommended in DKA (pH > 7)
Impaired myocardial
contractility Cerebral vasodilation Coma
pH < 6.9
50 to 100 mmol of sodium bicarbonate should be given as an isotonic solution (in 200 mL of water) every 2 hours
until the pH rises to ∼6.9 to 7.0. In patients with arterial pH >7.0, no bicarbonate therapy is necessary

17. PHOSPHATE AND MAGNESIUM
Correction usually not required
Periodic Monitoring

19. 74-year-old woman who is a known diabetic is brought to the ED by EMS with altered mental status. The
home health aide states that the patient ran out of her medications 4 days ago. Her BP is 130/85 mm Hg, HR
is 110 beats per minute, temperature is 99.8°F, and RR is 18 breaths per minute. On examination, she cannot
follow commands but responds to stimuli. Laboratory results reveal normal CBC Na 128 mEq/L, K 3.0 mEq/L,
Cl 95 mEq/L, Hco3 22 mEq/L, BUN 40 mg/dL, Cr 1.8 mg/dL, and glucose 850 mg/dL. Urinalysis shows 3+
glucose, 1+ protein, and no blood or ketones. After addressing the ABCs, which of the following is the most
appropriate next step in management?
A. Begin fluid resuscitation with a 2- to 3-L bolus of normal saline
B. Begin fluid resuscitation with a 2- to 3-L bolus of normal saline; then administer
10 units of regular insulin intravenously and begin phenytoin for seizure prophylaxis.
C. Administer 10 units of regular insulin intravenously; then begin fluid resuscitation
with a 2- to 3-L bolus of normal saline.
D. Order a computed tomographic (CT) scan of the brain; if negative for acute stroke,
begin fluid resuscitation with a 2- to 3-L bolus of normal saline.
E. Arrange for urgent hemodialysis.

21. COMPLICATIONS OF DKA AND HHS
• Hypoglycemia
• Hypokalemia
• Cerebral Edema
• AKI
• Venous Thromboembolism
• Rhabdomyolysis

22. A 47-year-old man presents with hypoglycemia. He is a known type 2 diabetic on glyburide.
Fingerstick glucose is 27 mg/dL. Twenty minutes after two ampules (50 g) of dextrose, his
glucose level is 29 mg/dL. Which of the following agents is indicated?
Answer: E. A patient with hypoglycemia from sulfonylureas, in addition to standard glucose
replacement, frequently requires treatment with an agent to inhibit further insulin release, such as
octreotide (a somatostatin analogue). Sulfonylureas are insulin secretagogues.
A. Adenosine
B. Epinephrine
C. Glucagon
D. Hydrocortisone
E. Octreotide

23. HYPOGLYCEMIA
Glucose is an obligate metabolic fuel for all tissues under physiologic conditions
Brain cannot synthesize glucose, store more than a few minutes’ supply as
glycogen, or utilize physiologic concentrations of circulating fuels effectively.
Clinical Hypoglycaemia
Whipple
Symptoms, signs, or both consistent with hypoglycemia.
A low reliably measured plasma glucose concentration.
Resolution of those symptoms and signs after the plasma
glucose concentration is raised

24. HYPOGLYCAEMIA
Neuroglycopenic symptoms are a direct result of brain glucose deprivation
comaseizure
psychomo
tor
abnormali
ties
behavioral
changes
cognitive
impairme
nts
Sympathoadrenal Trigger by hypoglycemia

25. HYPOGLYCEMIA-ASSOCIATED AUTONOMIC
FAILURE IN DIABETES

26. HYPOGLYCEMIA TREATMENT
15 – 20 Gm Sugar (PO, PR,IV)
Pure fructose does not cross the blood–brain barrier
15-20
mins
Glucagon, in a dose of 1.0 mg in adults, SC/IM
Or
150 µg repeated if necessary
Glycogen
depleted

27. DISPOSITION

28. Thank You