glucose management

1. Clinical Case…

2. HPI
40 yr old female brought to
ER with weakness, difficulty
breathing, weight loss and
slight confusion.

3.  ROS: No fever, cough, HA or diarrhea
 PMHx: limited per patient distress, sister thinks
she takes something for “her sugar and her
pressure”
 FHx: DM, HTN, CAD
 Social: occasional ETOH, former smoker,
denies any other drugs. Works as a waitress,
has been off the past 2 days due to illness. No
other sick contacts.
More History…

4. T 97 HR 120 RR 30 BP 100/60 SpO2 98% RA
Gen: sitting up, mildly confused, uncomfortable
HEENT: PERRL, dry mucous membranes
Pulm: Clear bilaterally, no w/r/r
CV: tachycardic, no murmur
Abd: scaphoid, soft, mild TTP diffusely
Ext: 2+ pulses, no clubbing
Neuro: A&O to self and place, occasionally confused, move all
extremities
Physical Exam

5. 650
122 20
3 10 1.4
92
41.5
12.6
13.3
127
UA: 3+ glu, 2+ ket, 100
pro, 2 RBCs, 0 WBCs
Ethanol: (-)
Utox: (-)
B-hydroxybutarate: 6
VBG: 7.04/30
N
77
L
12
M
11
E
0
B
0
Bands 0
Labs

6. Diagnosis?
Diabetic Ketoacidosis

7. {
Problems with
Glucose
Joy Mackey, MD
Dept of Emergency Medicine
Alpert School of Medicine, Brown University

8.  DKA
 A brief diversion on AKA
 HHS (aka HONK)
 Hypoglycemia
Objectives

9.  Overview
 Life threatening, acute onset.
 More common in Type I DM but can present in Type II
(esp new diagnosis).
 Clinical Presentation
 Polyuria, polydipsia, abd pain, Kussmaul respirations,
AMS, hypotension (due to prostaglandin dysregulation)
Diabetic Ketoacidosis

10.  Diagnosis
 Chem 7, UA, CBC, ABG/VBG, B-hydroxybutarate, EKG
 Elevated Glocose ( glu over 200)
 Electrolyte Abnormalities!!!
 HYPOkalemia
 1.5 meq/L
 HYPOnatremia
 Elevated Creatinine
 Differential: alcoholic ketoacidosis, renal failure, acute
lactic acidosis, tox: asa, toxic alcohols
Diabetic Ketoacidosis

11.  Treatment
 Fluids
 NS, at least 2L bolus
 Potassium
 Start replacing at 10 meq/hr when K <5.3
 Insulin
 0.1 U/kg/hr infusion . ONLY GIVE IF K>3.3
 Continue even when sugar ,250 until AG and ketosis
resolves, When BG <250, start D5 ½ NS
 Give long acting SQ insulin 1-2 hrs before stopping
infusion
 Glucose check q2H and potassium checks during tx
 Disposition: ICU
Diabetic Ketoacidosis

12.  Overview
 Typically seen in chronic alcoholics
 Starvation (sudden cessation of ETOH or food by
nausea/vomiting)
 Clinical Presentation
 Nausea, vomiting, abd pain
 SOB, tachycardic, tachypneic
 +/- pancreatitis or gastritis
 Diagnosis
 Chem 7, CBC, ABG/VBG, Amylase, lipase, UA, B-
hydroxybutarate
 Treatment
 D5 NS
 Thiamine 100mg
 Replace electrolytes (K+ and Mg2+)
Alcoholic Ketoacidosis

13.  Overview
 Life threatening, higher mortality than DKA
 More common in uncontrolled DM Type II,
 Usually has a precipitant event such as illness or
debilitated patient
 Clinical Presentation
 Insidious, elderly, presence of co-morbidities
 Weakness, anorexia, fatigue, nausea AMS,
seizures
 Progresses over days to weeks
Hyperosmolar
Hyperglycemic state

14.  Diagnosis
 Chem-7, ABG/VBG
 Glucose >600 (usually), serum
osmolarity >315, without a gap
or acidosis
Hyperosmolar
Hyperglycemic state

15.  Treatment
 NS bolus (15-20ml/kg in the first
hr, then titrate down)
 Identify underlying illness
 Replace electrolytes
 AFTER fluids, insulin infusion at
0.1U/kg/hr
 When glucose < 300, start D5 ½
NS instead of NS
Hyperosmolar
Hyperglycemic state

16.  Overview
 Typically due to iatrogenic med
effect, adrenal insufficiency
 Clinical Presentation
 Dizziness, nausea, diaphoresis,
AMS, focal neurological deficits
Hypoglycemia

17.  Diagnosis
 Fingerstick BG, chem-7
 Treatment
 If on long-acting antiglycemic
(i.e. sulfonureas): 1 amp D50 or
PO juice, admit for 24 hrs obs
with q4H glu checks
 If not on antiglycemics: 1 amp
D50 or PO juice, reassess
Hypoglycemia

18. Octreotide
Sulfonylurea Overdose
Used for sulfonylurea overdoses when more than 1-
2 boluses of D50W are ineffective to control
hypoglycaemia.
50-100 mcg SC/IV BID/TID, adjust according to
blood glucose
For IV, dilute in 50 mL 0.9% NaCl or D5W and
infuse over 15-30 minutes (may be given IV push
over 3 minutes)

19.  DKA is one of the most serious acute
complications of diabetes mellitus (DM).
 It can occur in both Type I and Type II DM
as well as gestational DM, with the highest
prevalence seen in patients with Type I
DM.
 DKA should be treated as a medical
emergency.
 DKA has a 10-20% mortality rate, HHNS is
10x higher
 Hyperosmolar hyperglycemic syndrome
(HHS) is a similar condition to DKA, but
more common in T2DM.
KEY POINTS

20.  Patients in DKA will often present with nonspecific
symptoms, including N/V and generalized
abdominal pain. Rarely, there is a fruity breath
odor (secondary to acetone development).
 Patients will often complain of the “Poly’s” –
polydipsia, polyuria, and polyphagia.
 Patients will ALWAYS be significantly fluid
depleted (may see orthostatic hypotension,
tachycardia, skin tenting, etc.).
 Classically for board exams, Kussmaul respiration
(fancy way to describe rapid, deep breathing) can
be seen in severe cases, secondary to severe
metabolic acidosis.

21.  The classic criteria for diagnosis of DKA is threefold:
 Hyperglycemia (usually between 350-500 mg/dL, with value
often <800 mg/dL)
 Anion gap metabolic acidosis (confirmed with ABG/VBG,
usually with pH < 7.30 or serum bicarbonate <15)
 Positive serum/urine ketones (confirmed with UA or specific
ketone test including acetoacetate, acetone, and β
 hydroxybutyrate)
 DKA patients are often hyponatremic, with profound
ketonemia and ketonuria. DKA rapidly develops <24 hours.

22.  Criteria for HHNS include: Diabetic patient with AMS, Severely
elevated glucose (usually >600), Minimal ketonuria or ketonemia,
Serum osmolality >320, Bicarbonate >15, or pH >7.3
 HHNS is another way of saying hyperglycemia + dehydration
leading to altered mental status (AMS). Patients are classically
older, more likely to be type 2 diabetics, and nursing home
residents.
 AMS can be generalized or have focal neurologic deficits. AKI is
common. Unlike DKA, it develops over days/weeks with minimal
to no ketoacidosis.
 Patients are often pseudohyponatremic, hypomagnesemic.
 Most importantly, HHNS patients have more of a fluid deficit-
incredibly often >100 mL/kg!
 Thromboembolic events more common in HHS (due to
hyperviscosity), and there is a 10x higher mortality than DKA.

23.  Important differential diagnoses:
 Alcoholic ketoacidosis (anion gap metabolic
acidosis without significant hyperglycemia)
 Hypoglycemia (altered mental status,
abdominal pain, and acidosis; fairly obvious
on initial fingerstick). Sepsis (sepsis should
be suspected in patients with hyperglycemia
and fever)
 Other things to think about: Intoxication (e.g.
methanol, ethanol, salicylates, isopropyl
alcohol, paraldehyde, ethylene glycol)

24.  IV access is crucial, as the first intervention is starting IV crystalloid
boluses, LR vs NS. LR.

 The goal of fluids is to correct both hypovolemia and
hyperosmolality.
 Most patients are profoundly dehydrated, and we administer rapid
fluid boluses while awaiting further lab studies before starting
insulin.
 Once fluid is running, correcting the sugar becomes the next
priority, which is achieved with IV regular insulin at 0.1 units/kg/hr
to tame glucose and close the anion gap.
 Be certain that the patient is not hypokalemic before giving insulin.
 Insulin boluses have fallen out of style as they studies in adults
have found neither significant benefit nor harm from using an
insulin bolus.
 There might be risk of cerebral edema. However, a pro-move in the
ED while you are waiting for the insulin drip (if it takes a while), is
to inject 10U regular insulin IV push if you find yourself waiting for
a long time for the drip.
 When the drip is started be aggressive about increasing it fast if no
rapid improvement.

25.  After a few hours, fluid replacement and insulin administration
depends more on the clinical presentation/state of hydration,
serum electrolyte levels, and I/O’s.
 The key electrolyte to evaluate is potassium! Replacement should
be initiated immediately if <3.5 mEq/L.
 If K+ between 5.5-3.5 mEq/L, 20-30 mEq of KCl should be given
along with insulin via IV fluids due to cellular shifts seen with
introduction of insulin.
 While the Na+ may look uncharacteristically low, like the K+, it is
typically due to pseudohyponatremia (glucose replaces Na as the
main ion of the blood).
 Hyponatremia often requires no treatment, and we recommend
close monitoring for improvement as treatment progresses.
 When glucose reaches ~250 mg/dL, we advise switching to IV
fluids that contain dextrose.

26.  Bicarbonate?
 What patients need is maximally aggressive management of their
DKA (fluids and more insulin).. There is no evidence that bicarbonate
works as a treatment of ketoacidosis.
 Do not give if pH >6.9. If pH is below this and patient is in extremis,
giving 100 mEg might not be a bad idea, but there is minimal
evidence for it.
 In fact, raising bicarbonate levels in theory will reduce respiratory
drive and possibly worsen the metabolic acidosis.
 This whole area is controversial, and we advise no bicarbonate unless
pH <6.9 and the patient is clinically in extremis (not sitting up in bed
and talking).
 Resolution— The hyperglycemic crisis is considered to be resolved
when the following goals are reached:
 Ketoacidosis has resolved: normalization of the serum anion gap (less
than 14 mEq/L) and blood beta-hydroxybutyrate levels undetectable.
 The patient is able to eat.

27.  The Diabetes prevalence of Belize is
15.9 (% of population ages 20 to 79)
with a global rank of 15.
 Belize’s prevalence similar to:
 Guam, United Arab Emirates, Palau,
Egypt, Guyana, Solomon Islands,
Lebanon, Turkey
BELIZE

30. QUESTIONS ?