This document discusses glucose homeostasis and diabetic emergencies from an emergency perspective. It provides guidance on assessing altered mental status, including checking a blood sugar level. It describes insulin and its role in glucose metabolism. Diabetic ketoacidosis and hyperglycemic hyperosmolar state are life-threatening disorders that can result from lack of insulin or inability to use insulin properly. Proper treatment involves fluid resuscitation and insulin therapy while closely monitoring electrolytes. Hypoglycemia is also covered, noting it can result if insulin levels are too high.

1. Glucose homeostasis
Dr Anand.Tiwari
Head of dept.ICU
Wanowrie Ruby hall

2. Emergency prespective
• When do you advise a blood sugar ?

3. • Brain is the biggest user of glucose
ALTERED MENTAL STATUS

4. Pinprick for BSL
• Altered glucose metabolism should
be considered in the
• differential diagnosis of all patients
with mental status changes,
• neurologic deficits, and severe
illness
Do not neglect the initial assessment of ABC

5. Insulin and glucagoan

6. Toronto university…..1921

8. Insulin
• Hormone required to transfer glucose from
the blood to the tissues and the cell where it
can be used as fuel.
• Anabolic hormone
• Ant catabolic action
• Liver acts as a buffer

9. The Diabetic patient
• Diabetes is a medical condition when
persons pancreas will no longer produce an
adequate supply of insulin or when the
body loses ability to utilize insulin properly

10. Gluocose tolerance curve

11. Glycosylated Hemoglobin
• 6.5%
• 7%
• 7.5%

12. Pathophysiology of Diabetic Emergencies
• type 1 diabetes (previously known as
juvenile onset,
• ketosis-prone, insulin-dependent, or
brittle diabetes) or
• type 2 diabetes (previously, adult-
onset, non-ketosis-prone,
• non-insulin-dependent, or obesity-
related diabetes
• T3Gestational

13. • SUGAR CONTROL IN DIABETICS
• DIET CONTROL
• INSULIN
• ORAL HYPOGYCEMIC DRUGS

14. Diabetes video

15. Diabetic emergencies
• HYPERGLYCEMIA
• HYPOGLYCEMIA

16. • You receive a patient in ER who is
obtunded,what is your approach to the
patient /?????????????

17. Emergency care
• SAMPLE
• What did you last eat?
• Do you take diabetic medication?
• Have you taken your medication as
prescribed?

18. life-threatening disorders of glucose
metabolism.
• DKA
• HHNC
• hypoglycemia
Atherosclerosis
Infection
Retinopathy
Cataract
Hypertension
Ckd
Neuropathy
Foot

19. Stop and review
Q --HYPOGLYCEMIA IF LEFT
UNTREATED WILL RESULT IN
• A.-INSULIN COMA
• B-DIABETIC SHOCK
• C-DIBETIC COMA
• D-INSULIN SHOCK

20. • TYPICAL SYMPTOMS OF
HYPOGLYCEMIA OCCURS
BELOW?/?
• A-120mg%
• B-80mg%
• C-50mg%
• D-400mg%

21. • Q- which of the following is
contraindication for administrating oral
glucose to a known diabetic patient?
• A-low blood glucose reading
• B-unresponsive patient
• C-patient able to swallow easily
• D-patient taken insulin recently

22. Insulin deficiency
• in lipolysis and unrestrained fatty acid
oxidation, producing
• acetone,
• β-hydroxybutyrate,
• acetoacetate—

23. Intracellular
Interstitial
Intravascular
2/3 1/3
3/4 1/4
ECF osmolality = ICF osmolality
K, ATP
Creatinine PO4
phospholipids
Na, Cl
HCO3

24. Osmotic diuresis
• The glucose remains largely in the
extracellular
• space and shifts water osmotically from
the intracellular compartment.
• of the renal tubules for glucose has a
maximum of approximately 200 mg/min,
an osmotic diuresis occurs, with water lost in
• excess of salts.

25. DKA
• Hyperglycemic condition in which absence
of insulin causes the body to metabolize
other sources of energy such as fat .The
blood becomes acidic and condition may
result in fruity breath odor and altered
mental status
• (

26. Kussmaul respiration
• )
• Respiration that are both rapid and
deep seen in patient with extreme
hyperglycemia associated with the
fruity odor of acetone.

27. Enumerate medical causes of
•
• ACUTE ABDOMEN???

28. Diabetic ketoacidosis
• Dyspnea
• Normotension
• Hypo- and hyperthermia
• Nausea
• Tachycardia

29. S/symptoms
• Lethargy to coma
• Vomiting
• Tachypnea
• Fruity breath
• Abdominal pain
• Abdominal tenderness
• Orthostatic
• Cerebral edema

30. Lab paradox
• nitroprusside reaction commonly used
to detect ketone bodies
• detects acetoacetate much better than
acetone and does
• not react with β-hydroxybutyrate at all.
Particularly in severe
• DKA, β-hydroxybutyrate is the
predominant ketone,

31. Laboratory findings
• 1. Serum glucose level >300 mg/dL
• 2. pH <7.35, pCO2 <40 mm Hg
• 3. Bicarbonate level below normal with an
elevated anion gap
• 4. Presence of ketones in the serum

32. What next
• CHECK ANION GAP
• Causes of raised anion gap
• MUDPIES

33. Differential diagnosis
• A. Differential diagnosis of ketosis-causing conditions
• 1. Alcoholic ketoacidosis occurs with heavy drinking
• and vomiting. It does not cause an elevated
• glucose.
• 2. Starvation ketosis occurs after 24 hours without
• food and is not usually confused with DKA because
• glucose and serum pH are normal.

34. Treatment of diabetic ketoacidosis
• Fluid resuscitation
• Which fluid???
• When to introduce 5% dex

35. Insulin
• loading dose consists of 0.1 U/kg IV
• . then infused at 0.1 U/kg per hour.
• glucose decline does not
• exceed 100 mg/dL per hour.
• 2. The insulin infusion rate may be decreased
when the bicarbonate level is greater than 20
mEq/L, the anion gap is less than 16 mEq/L, or the
glucose is <250 mg/dL.

36. Potassium
• deficit is between 300 and 500 mEq
• potassium replacement is 20 mEq/h, but
• hypokalemia
. All patients should receive potassium replacement,
• except for those with renal failure, no urine output,
• or an initial serum potassium level greater than 6.0
• mEq/L.

37. Sodium.
• . For every 100 mg/dL that glucose is
elevated, the sodium level should be
assumed to be higher than the measured
value by 1.6 mEq/L.

38. Other electrolytes
• Phosphate. Diabetic ketoacidosis depletes phosphate
• stores. Serum phosphate level should be
• checked after 4 hours of treatment. If it is below 1.5
• mg/dL, potassium phosphate should be added to the
• IV solution in place of KCl.
• F. Bicarbonate therapy is not required unless the
• arterial pH value is <7.0. For a pH of <7.0, add 50
• mEq of sodium bicarbonate to the first liter of IV fluid.
• G. Magnesium. The usual magnesium deficit is 2-3 gm.
• If the patient's magnesium level is less than 1.8
• mEq/L or if tetany is present, magnesium sulfate is
• given as 5g in 500 mL of 0.45% normal saline over 5
• hours.

39. Say no to soda bicarbonate??
• Therapy of DKA and HHNC requires
replacement of deficits of
• fluids, electrolytes, and insulin

40. Freezing point depression method
• Osmolarity (mOsm/L) = 2 × [sodium]
• + [glucose]/18 + [BUN]/2.8 +
[ethanol]/4.6

41. disastrous consequences of
aggressive
therapy
• —cerebral edema,
• pulmonary edema,
• hypoglycemia,
• hypokalemia, and
• hyperchloremic metabolic acidosis.

42. Why decompensation?
Search for Infection

43. BS control in acute illness
• Maintaining BS between 80-100 mg/dl
• Surgical ICU (Van den Berghe et al, 2001)
– In-hospital mortality 11 to 7%
– Reduction in severe infections, polyneuropathy and
organ failure
• Medical ICU (Van den Berghe et al, 2006)
– Prevent acute renal failure, accelerated weaning from
ventilator, reduced ICU and hospital stay
– Mortality reduced in people who stayed in icu for more
than 3 days
• Control population had BS control once BS > 215
mg/dl

44. Review questions
• All of the following pathways occur as diabetic
• ketoacidosis develops EXCEPT
• (A) hyperglycemia → glycosuria → dehydration
• and loss of electrolytes
• (B) hyperglycemia → cell dehydration → altered
• level of consciousness
• (C) insulin and glucagon deficiency → increased
• hepatic gluconeogenesis
• (D) lipolysis → ketosis → acidosis
• (E) muscle breakdown → azotemia →
• loss of sodium

45. Which of the following statements is TRUE regarding
administration of sodium bicarbonate solution during
the management of diabetic ketoacidosis (DKA)?
• (A) It prevents paradoxical spinal fluid acidosis
• and cerebral edema
• (B) It shifts potassium ions extracellularly and
• corrects the hypokalemia
• (C) It shifts the oxyhemoglobin dissociation curve
• to the right, facilitating off-loading of oxygen
• at the tissue level
• (D) Complications include rebound alkalosis and
• sodium overload
• (E) It is recommended in all DKA patients with
• severely altered levels of consciousness

46. All of the following are appropriate treatments
for
DKA EXCEPT
• (A) administering 3 to 5 L normal saline in the
• first 4 to 6 h
• (B) replacing the 3 to 5 mEq KCl/kg deficit
• gradually over the first 2 to 3 days
• (C) infusing insulin at 0.1 U/kg/h after the initial
• bolus is given
• (D) stopping insulin administration when glucose
• levels fall to 250 mg/dL
• (E) administering phosphate if levels fall below
• 1.0 mg/dL

47. Which of the following statements concerning
hyperosmolar
hyperglycemic nonketotic syndrome (HHNS) is
TRUE?
• (A) The mortality rate of HHNS is less than that
• of DKA
• (B) HHNS and DKA are easily distinguishable
• (C) A majority of HHNS patients present
• with coma
• (D) Metabolic acidosis excludes the diagnosis
• (E) Seizures occur in up to 15 percent of patients
• with HHNS

49. • What is the MOST common cause of
hypoglycemia
• in patients presenting to the ED?
• (A) First time presentation of diabetes
• (B) Alcohol related
• (C) Oral hypoglycemics
• (D) Insulinoma
• (E) Liver failure

50. Which of the following statements
regarding hypoglycemia
is FALSE?
• (A) Counterregulatory hormones are released in a
• hypoglycemic state
• (B) Hypoglycemia causes both autonomic and neuroglycopenic
• symptoms
• (C) Hypoglycemic patients commonly present with
• altered levels of consciousness, lethargy, confusion,
• or agitation
• (D) Hypoglycemia is diagnosed when the blood
• glucose is less than 60 mg/dL
• (E) Glucagon is ineffective in the treatment of
• alcohol-induced hypoglycemia

51. • A patient presents to the ED and has the following
• laboratory values: sodium 139 mEq/L, potassium 4.1
• mEq/L, chloride 112 mEq/L, bicarbonate 15 mEq/L,
• blood urea nitrogen (BUN) 22, creatinine 1.5, and
glucose 180. All of the following could be the etiology of
• these laboratory findings EXCEPT
• (A) salicylates
• (B) renal tubular acidosis, type II
• (C) acute diarrhea
• (D) ureterosigmoidostomy
• (E) pancreatic fistula

52. • What is the calculated osmolarity for the patient in
• question 300?
• (A) 157 mOsm/L
• (B) 274 mOsm/L
• (C) 296 mOsm/L
• (D) 310 mOsm/L
• (E) 347 mOsm/L

53. • The etiologies of this patient’s normal AG
• (hyperchloremic) metabolic acidosis can be
remembered by a helpful mnemonic,
• HARDUP: H for hypoaldosteronism (Addison’s
disease), A for acetazolamide, R for renal
• tubular acidosis, D for diarrhea, U for
ureterosigmoidostomy, and P for pancreatic
fistula.