This document discusses the management of hyperglycemic crises including diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). It provides guidelines on the identification and treatment of these conditions. It presents a case study of a patient with vomiting and elevated blood glucose and ketones who is diagnosed with DKA. It covers the diagnostic criteria, precipitants, signs and symptoms, pathophysiology, treatment including fluid resuscitation and insulin therapy, complications, and discharge planning for DKA and HHS. Hypoglycemia is also discussed including causes, outcomes, and treatment approaches.

1. Hyperglycemic crises and
Hypoglycemia
Kerolus Shehata, MD
“Focused, practical and guidelines-directed approach”

2. Learning Objectives
 Identification and discussion of guidelines-directed
management of the three main acute diabetic
complications (Hypoglycemia, DKA, HHS)

3. Case No. 1
 A 45 year old woman with diabetes who presented to
the ED c/o vomiting x3 days. She had been unable to
tolerate any food, so she was drinking Gatorade and
Vitamin Water trying to stay hydrated. She
previously presented to another ED 2 weeks ago with
axillary abscesses and was given an antibiotic with
little improvement.
Na 131 Cl 92
K 5.7 HCO3 13
BUN/Cr 33/2.7 B-HBA 8.5
Glucose 1194 PH 7.24

4. What needs to be addressed?
 What is the differential diagnosis?
 Will she be admitted to the floor or MICU?
 Any other lab tests/Imaging studies ?
 What will be the inpatient management/care plan?
 What will be the pre-discharge plan?

5. The magnitude of the problem
 More than 100 million U.S. adults are now living
with diabetes or prediabetes
 In 2014, 207,000 ED visits with hyperglycemic crises
 In 2014, 168,000 hospital admissions with DKA
 The direct and indirect annual cost of DKA
hospitalizations is about 2.4 billion US dollars.
 The incidence of diabetes and its complications (and
hence the healthcare cost) is expected to increase
dramatically by 2030.

6. Inpatient Glycemic Targets
Non-ICU setting ICU setting
• SQ basal/bolus regimen is preferred
• Pre-meal BG: <140
• Random BG: <180
• More stringent targets in stable
patients
• Less stringent targets in the elderly
and in patient with multiple co-
morbidities
• Insulin infusion is preferred
• Goal BG: 140-180
• BG <110 is not recommended

7. Diabetic Keto-Acidosis (DKA)
Mild DKA Moderate DKA Severe DKA
• PH (A or V) 7.25-7.30 7.0-7.24 <7.0
• HCO3 15-18 10-14 <10
• Mental status Alert More drowsy Stupor/Comatose
Is there a BG cut-off to diagnose DKA? (euDKA)
Diagnostic criteria if DKA:
1- Diabetic  BG>250
2- Keto  +ve Ketones (Urine and serum)
3- Acidosis (Metabolic, High AG)  PH<7.30, HCO3 <18
• Keroacids productions in these cases is indicative of absolute insulin deficiency

8. Hyperosmolar Hyperglycemic State (HHS)
 You need little insulin to prevent lipolysis and fatty
acids oxidation which yields Ketocaids.
 You need more insulin to stimulate glucose entry
to the cells for utilization.
 In HHS, you have enough insulin to prevent
Ketocaids production, but not enough for cellular
utilization of glucose. So, HHS is a state of relative
insulin deficiency.

9. Diagnostic criteria of HHS
 Hyperglycemic  >600
 Hyperosmolar  >320
 Non-DKA  PH>7.30, HCO3>15, no or minimal
ketones in urine or serum
• Generally: DKA occurs more in type I DM, HHS occurs more in type II
DM. They can be the first presentation of either type.

10. Pathophysiology of Hyperglycemic Crises

11. Signs and symptoms of DKA/HHS
DKA HHS
Timeline <= 24H Several days
GI (N/V/abd. Pain) + +/-
Mental status Depending on severity
(Generally more awake)
Generally stupor or
comatosed
Dehydration + /++ ++++
Fruity odor +/- -
Kussmaul’s breathing + -
• Never forget to look for the precipitant

12. Extras…
What are the causes of Ketosis +/- Ketoacidosis?
1. Diabetic (DKA)
2. Alcoholic
3. Low CHO diet (Ketogenic diet)
4. Dehydration from any reason (Fasting Ketosis)
5. Strenuous exercise
 Ketoacids: B-HBA, Acetoacetic acid
 Acetone: ketone body, not an acid
 Bedside Ketone monitoring is approved to monitor
the resolution of DKA in the UK

13. Precipitants of DKA/HHS
 Infections/Inflammation
 Insulin Ignorance
 Insulin pump failure
 Intoxication
 Ischemia/Infarction (Cardiac, Cerebral, Bowel)
 Pregnancy
 Medications especially steroids/SGLT2-inhibitors
 Fasting: fasting ketosis

14. To sum up: DKA vs HHS
Pure DKA Pure HHS
More common in type I DM More common in type II DM
Absolute insulin deficiency Relative insulin deficiency
Mortality is about 2% Mortality is about 20% (Comorbidities)
Lesser degree of dehydration Profound dehydration
More GI s/s More CNS s/s
BG >250 BG>600
PH: <7.3-High AG PH: >7.3-Normal AG
Serum Osmolality <320 Serum Osmolality >320
High serum and urine ketones No or minimal serum and urine ketones

15. Work up
To diagnose DKA/HHS To identify the precipitant
BMP CBC, UA, B-HCG (In females)
ABG/VBG Blood, urine +/- sputum cx
Serum Osmolality Amylase/Lipase
Serum B-HBA UA-UDS
Troponin - EKG
CXR, CT-brain wo/contrast  MRI Mg – PO4
Abdominal US, CT abdomen/Pelvis Alcohol level, Toxic alcohols
CXR HBA1c
Tailor what you order based on your clinical suspicion (Cost-effective)

16. Let’s go back to our case
• Is the patient hyponatremic?
• What is the AG? (Na-Cl-HCO3). Remember to use the measured Na
• What is “Corrected AG”?
• What is the calculated serum Osmolality?

17. Fluid replacement
“Amount, Type and rate”
 Amount will depend on:
1. Clinical evaluation (Degree of dehydration)
2. Comorbidities e.g. CHF, ESRD…etc.
3. Corrected serum sodium
 Upon confirmation of DKA o HHS Dx and if not C/I, patient should be given 1L NS
bolus (Usually I one hour), can be repeated depending on the aforementioned
factors.
 Depending on corrected Na, you will start Maintenance IVF (NS or ½ NS) at rate
between 250-500 depending on the degree of dehydration and other comorbidities.
 Once F/U BG reaches 200 or less in DKA (300 or less in HHS), change NS or ½
NS to D5-1/2 NS (+/- KCL 20 mEq) at rate of 150-250 cc/hr to avoid hypoglycemia
(Remember that your patient is still NPO and Insulin drip is still running)

18. POTASSIUM
 Total body K will be decreased in most of DKA/HHS
 Initial labs may show Normo- or even hyperkalemia
related to Insulin deficiency (Re-distribution) and
the acidosis (in case of DKA)
 NEVER to start Insulin without knowing (K).
 Goal K: 4-5
K 5.3 or more Can start insulin drip. Recheck K in 2h
K 3.3 – 5.2 Can start Insulin drip, but every liter of IVF (NS or ½ NS)
must have 20-30 mEq KCL (better to use the premixed fluid)
K 3.2 or less NO INSULIN. Give KCL 20-30 mEq per hour (May need
central line) and recheck K every hour till >3.2

19. Insulin
 Remember check K first
 Initially: DKA/HHS must be placed on Insulin Drip
(Regular Insulin), to be titrated as per nursing
protocol depending on the hourly BG check
When do we given IV insulin bolus (0.10-0.14
u/Kg)?
1. Sometimes, initially before the drip. No benefit
2. If BG decreases <10% in 1h after starting the drip

20. Insulin…Cont’d
 While on Insulin drip and maintenance IVF, your must
get BMP (+/- ?Phosphorus) q2-4H, Serum Osmolality
(In HHS)
 Look for K, HCO3, AG (+/- BUN/Cr, PO4)
When will you stop the insulin drip?
1. Normalization of the AG
2. HCO3 >17
3. Patient tolerates PO intake (at least 50% of the tray)
(Which by default means that he is awake and alert
and hemodynamically stable)
4. After 2 hours of starting bridging with a long acting
Insulin (Glargine)

21. Insulin…Cont’d
 What is a “Safe” BG drop rate on Insulin drip-
DKA/HHS protocol?
 No clear cutoff (? 100)
 Effective insulin drip rate should drop BG by at least
50-75 mg/dl/hr
 The idea is that rapid shift in serum osmolality can
precipitate brain edema “more in children”)
 The concept of Insulin bridging is to keep a steady
state insulin concentration in the plasma upon
transitioning from IV to SQ insulin.

22. Insulin Bridging
Which SQ insulin will we use?
• Long acting (Glargine)
• If remained stable and tolerated subsequent meals, cover with pre-meal short
acting along with a sliding scale.
What is the dose?
• Calculate how many units of IV regular insulin they were given in the last 24H
(That will represent TDD  Divide it to basal/bolus/SSI regimen)
• If newly diagnosed DM (Insulin naïve)  Wt-based basal/bolus SSI regimen
(0.5-0.8 u/kg)
• If already on Insulin at home, use 50-75% of their TDD while inpatient
N.B. Insulin regimen, especially if
naïve, is a trial and error and actually
that is the reasoning being putting SSI
and hypoglycemic precautions.
Undershooting here is better than
overshooting

23. Bicarbonate and Phosphorus
 Don’t use NaHCO3 unless PH is <6.9…May worsen the
intracellular acidosis and precipitate or worsens cerebral
edema especially in children.
 May use drip or pushes PRN
 Dose: 100-150 mmol (2-3 amp) over 2 H…along with
KCL 20mEq. Can be repeated
 F/U ABG in 2 H along with serum K
 Goal PH: more than 7.0-7.1
 Phosphate shouldn’t be routinely checked
 Unclear significance of PO4 replacement unless (Patient
is severely acidotic or on MV or level <1.0)
 IV PO4 carries the risk of hypocalcemia

24. To sum up: DKA/HHS Protocol

25. Complication of Hyperglycemic crises
 Hypoglycemia (upon treatment)
 Thrombosis (DVT)..Prothrombotic state
 Electrolyte disturbances: Hypo-K, Mg, PO4
 Cardiac arrhythmias
 Cerebral edema (Mainly in children/Adolescents)
 Pulmonary edema and ARDS (Rare with rapid BG
drop)
 Rarely, cerebral hemorrhage and Intestinal necrosis
 Pancreatitis (Precipitant and a consequent)
 Rarely with HHS, Malignant hyperthermia-like
syndrome with Rhabdomyolysis
 Death

26. Downgrading and Pre-discharge planning
 Always get Endocrinology on board
 Always get a Diabetes educator on board
 Always make a F/U appointment with
PCP/Endocrinology clinics in 1 w after D/C
 If needed, Social work to assist with
medications and insulin supplies

27. Hypoglycemia
Hypoglycemia unawareness: Hypoglycemia associated autonomic failure

28. Predisposing Factors for Hypoglycemia
 Mismatch between insulin administration and CHO
absorption (common on the floor or in cases of
gastroparesis)
 Higher insulin dosing (Overshooting)
 Decreased PO intake
 Decreased insulin requirements (ESRD, Liver cirrhosis)
 Hypothyroidism, Hypopituitarism, Primary adrenal
insufficiency
 Alcohol consumption/Intoxication
 Malnutrition

29. Outcomes of hypoglycemia
 Full gross recovery (?)
 Encephalopathy
 High long term risk of dementia, cognitive
dysfunction and ataxia
 Sudden cardiac death: Dead in bed syndrome (in
Type I DM)

30. Management of hypoglycemia
 Mild to moderate: Carb-containing beverages, 3-4
glucose tablets, glucose oral gel
 Severe: IV D50 25 gm push (1/2 – 1 amp), remember
to recheck in 15-30 min
 If persistent hypoglycemia: D10 drip
 If no IV access: IM or SQ glucagon (0.5-1 mg) 
causes frequent N/V
 If resistant hypoglycemia to D50 or requiring high
rate of D10 maintenance, you can try Octreotide drip
or Steroids (Not EBM)
 Sulfonylureas can cause prolonged hypoglycemia
(Even more than 24 H)

31. Thank you