Disorders of Carbohydrate Metabolism.

1. ADNAN ALI
MBBS, MD
EMERGRNCY SPECIALIST
Disorders of Carbohydrate
Metabolism.

2. Disorders of Carbohydrate
Metabolism.
- INCLUDES
- Diabetic ketoacidosis
- Hyperosmolar Hyperglycemic
state(HHS)
- Hyperglycemia
- Hypoglycemia
- Lactic acidosis
- Alcoholic ketoacidosis

3.  Most CH metabolism disorders related to Diabetes
mellitus
 a broad spectrum of Emer. conditions
 Toxin ingestion, Cardiovascular diseases, multisystem
trauma, CV diseases, my mimic or exacerbate these
conditions.
 Clinical appearance variation
 From significant mental disorders to well appearance
while at edge of metabolic decompensation.

4. Most common acute life threatening complication
of Diabetes.
Commonly type 1 DM, may occur in type 2
Diabetic ketoacidosis

5. pathophysiology

7. Criteria for diagnosis
 Patients who Arterial PH < 7,3
 Serum Glucose >250 mg/ dL
 Serum Bicarbonate =/< 15 mEq/L
 Ketoneuria or ketonemia
 an anion gap >10

8. Causes diabetic ketoacidosis
 Omission or reduced daily insulin injections
 Dislodgement/occlusion of insulin pump catheter
 Recent or current infection of any type (most common)
 Pregnancy
 Hyperthyroidism
 Medications: steroids, thiazides, antipsychotics,
sympathomimetics
 Heat-related illness
 Cerebrovascular accident
 GI hemorrhage
 Pulmonary embolism
 Acute or acute-on-chronic pancreatitis
 Major trauma
 Surgery
 Acute coronary syndrome or myocardial infarction
 Ethanol or drug abuse/ Gastroenteritis

9. CLINICAL FINDINGS

10. Typical findings include:
 general fatigue and weakness
 abdominal pain( pseudoperitonitis)
 Kussmaul's respirations (rapid deep respirations
attempting to compensate for acidosis).
 fruity or acetone-like odor
 polyuria, polydipsia and polyphagia
 nausea and vomiting are found in up to 25% of
patients
 Mental status changes ranging from mild

11. Investigation
Routine lab
 CBC
 RFT
 RBG
 UG
 ABG
 Radiological imaging
 CXR
 Other
 ECG
 Coagulation profile

12. 1- Key findings
 serum glucose ≥ 250 mg/ dL
 serum ketones or ketonuria
 serum bicarbonate ≤ 15 mEq/L
 and arterial pH < 7.3
 (Arterial blood gas determination can be limited to
patients with an uncertain diagnosis or respiratory
concerns. Venous blood is an acceptable
alternative. The pH value is usually 0.03 lower than
that of arterial blood. This is especially useful for
repeated pH determinations.

13. 2- Serum Potassium
 initial serum potassium is unpredictable of real
potassium status
 Acidosis drives potassium out of the cells
causing a relatively higher serum potassium level
despite total body deficits that may be as much
as 3-5 mEq/kg.
 the determination of serum potassium should
precede insulin therapy.

14. Serum potassium
 If serum potassium is initially low, insulin
administration will exacerbate the situation by
facilitating the cellular entry of potassium.
 The rapid development of severe hypokalemia
may cause lethal arrhythmia

15. 3- Serum sodium
 Significant diuresis and emesis frequently lower
serum sodium
 Osmotic pressure from glucose also dilutes the
serum and fictitiously lowers the reported sodium
value.
 Sodium deficits may approach 7-10 mEq/kg;
however, rapid correction with increasing
osmolality may precipitate cerebral edema,

16. 4- Serum phosphate
 Serum phosphate values may be normal or
elevated
 Routine phosphate repletion does not improve
outcome in DKA
 hypophosphatemia (<1 mg/dL), however, may
cause skeletal, cardiac, and respiratory muscle
depression
 Phosphate should be replaced in this
circumstance. This can be done by using
potassium phosphate as 1/3 of potassium

17. 5- Other important laboratory
findings
A.Anion Gab
 useful to assess severity of acidosis and to follow
progress of therapy
 Anion Gab = [Na]- [Cl] + [HCO3]
 Normal values are 8- 16

18. 5- Other important laboratory
findings
 B- serum osmolality:
= 1.86[Na]+(glucose/18)+(BUN/2.8)
 osmolality values above 340 mOsm/kg usually result in
mental status changes.
 Below this value, other causes for lethargy or coma
should be investigated.
 This value may also be used to diagnose hyperosmolar
hyperglycemic state (HHS) and ingestions of ethanol,
ethylene glycol, or other alcohols.

19. 5- Other important laboratory
findings
 C serum ketones:
 The laboratory determination of serum ketones is
not always reliable as a diagnostic test
 The primary ketone body formed in DKA initially is
β- hydroxybutyrate. However, standard ketone
assays measure only acetoacetate

20. 5- Other important laboratory findings
 D- Blood urea nitrogen and
creatinine
 Their levels may be elevated because of
severe dehydration, acute tubular
necrosis, or renal failure.
 In these circumstances, establish urine
output prior to initiating potassium
repletion

21. HYPEROSMOLAR HYPERGLYCEMIC
STATE
(HHS)

22. ESSENTIALS OF DIAGNOSIS
 Most symptoms relate to severe dehydration
 Absence of acidosis, small or absent serum
ketones, and hyperglycemia usually ≥ 600 mg/dL
 Kussmaul's respirations and abdominal pain are
unusual findings

23. General Considerations
 patients with HHS have sufficient insulin activity
to prevent lipolysis and ketogenesis
 HHS results from
 gradual diuresis, resulting in severe dehydration
and electrolyte depletion without significant early
symptoms.
 This leads to profound electrolyte deficiencies and
eventually mental status changes.

24. General Considerations
 HHS is most commonly seen in older patients and
 oftenly caused by physiologic stressors such as
 infection
 myocardial infarction
 cerebrovascular accident
 trauma
 decreased access to water
 and drug effects or interactions

25. History
 Risk factors;
 Age> 65 years
 change in diabetes regimen
 addition of medications that may elevate glucose
levels (e.g., corticosteroids, thiazides,
anticonvulsants, sympathomimetics)
 recent or current infection, and dementia.

26. Symptoms and Signs
 polydipsia, polyuria, or polyphagia;
 generalized weakness;
 altered mental status (clouded thinking to
confusion to lethargy or coma);
 dry mucous membranes;
 poor skin turgor;
 and delayed capillary refill.
 Abdominal pain is not a typical finding in HHS (in
contrast to DKA);

27. Laboratory Findings
 Key laboratory findings—Key findings to diagnose
HHS and differentiate it from DKA are as follows:

28. Laboratory Findings
 Serum glucose ≥ 600 mg/dL.
 Urine or serum ketones are small or absent (a
small amount of ketone may be detected
secondary to starvation.)
 Glucosuria is prominent.
 Serum bicarbonate is usually > 15 mEq/L.
 pH is usually > 7.30.
 The anion gap may be variable depending on
precipitating cause but is usually ≤ 10.
 Serum osmolality is ≥ 320 mOsm/kg.

29. Serum sodium
 In the early stages of HHS, serum sodium
findings are similar to those in patients with DKA.
 Urinary losses and fluid shifts out of the cell and
into the extracellular compartment create
hyponatremia usually 125-130 mg/dL.
 Correction for hyperglycemia with the addition of
1.8 mg/dL sodium per 100 mg/dL of glucose
represents a more accurate value.

30. Serum potassium
 Serum potassium levels will most commonly be
normal or low, unless renal failure is present.
 Total body deficits are often 4-6 mEq/Kg or as
much as 500 mEq total.

31. Blood urea nitrogen and
creatinine
 Blood urea nitrogen (BUN) is often markedly
elevated.
 Gastrointestinal bleeding may also elevate BUN
and is a possible precipitating cause of HHS in
elderly patients

32. Treatment

33.  Treatment of DKA and HHS is very similar
 Continuous monitoring of vital signs, mental
status, and laboratory parameters is essential.
 A flow sheet may be helpful during resuscitation
due to the complexity of treatment and need for
frequent therapeutic changes

34. Resuscitation Issues
 Standard airway management is indicated
 Hypoxia should trigger an investigation for
aspiration, pneumonia, or pulmonary edema.
 Oxygen therapy is indicated for all DKA or HHS
patients via techniques adequate to maintain
oxygen saturation above 96% or Po2 ≥70 mm

35. Fluid Therapy
 Adequate fluid replacement is the most important
initial treatment of DKA and HHS.
 Fluid therapy is dictated by three parameters:
vital signs, corrected serum sodium, and serum
glucose
 Overall fluid deficits approach 6-10 L in most
patients.
 Large-bore (≥18-gauge) intravenous lines are
essential.
 Central venous access may be indicated.
 Hypotension should prompt a bolus of 1-2 L of

36. Fluid Therapy
 Caution: Cardiogenic shock and renal failure
complicate crystalloid resuscitation.
 Reassess patients frequently for adequate urine
output and signs of pulmonary edema or congestive
heart failure.
 Invasive hemodynamic monitoring is indicated in very
select cases to facilitate fluid management if
cardiogenic shock is present.
 During fluid Therapy
 Serum electrolytes including potassium, bicarbonate,
and sodium should be monitored every 1-2 hours along
with
 hourly glucose determination.
 The calculated serum osmolality should not decrease

37. Fluid Therapy
 Usually 1-1.5 L of 0.9% saline is infused over the first hour
while initial laboratory values are determined. Subsequent
infusion can be decreased to 500 mL/h, then 250-500 mL/h,
then 150-300 mL/h as the hydration status improves.
 If the serum sodium is high normal or high, 0.45% saline is
recommended after initial fluid boluses to avoid severe
hypernatremia. If serum sodium is low or low normal, 0.9%
saline should be continued.
 Once serum glucose reaches approximately 250 mg/dL, 5%
dextrose in 0.45% NaCl is the fluid of choice at a rate of 250
mL/h; alternatively use 5% dextrose in normal saline if the
corrected serum sodium remains low.
 The clinical relevance of the urine output is unreliable
while glucose levels remain high due to osmotic diuresis.
Once glucose levels approach normal, urine output may
be used to guide therapy; 30-50 cc/h is considered
adequate.

38. Potassium:
 Potassium repletion may begin once urine output is
confirmed and an initial potassium level is determined.
 With target levels of 4.0-5.0 mEq/L the following algorithm is
usefull
 If the serum potassium is 3.3 mEq/L or less, withhold insulin
therapy and give potassium replacement.
 If the serum potassium is 5.0 mEq/L or more, hold potassium
repletion and recheck the serum potassium in 1-2 hours.
 If levels are significantly elevated (above 6 mEq/L) or ECG
changes are noted, a regular insulin bolus of 8-12 units can
be given along with other standard treatments for
hyperkalemia
 Assume a deficit of about 100 mEq potassium for each 1

39. Insulin Therapy
 Insulin therapy should be delayed if the potassium level is less
than 3.3 mEq/L until the potassium level is rising
 continuous infusion of regular insulin at 0.1 Unit/kg body
weight per hour is the treatment of choice.
 After the serum potassium determination, a bolus of 0.1-0.15
Unit/kg body weight of regular insulin may be considered (not
recommended in pediatric patients).
 If glucose is not decreasing by at least 50-70 mg/dL/h, the
insulin dosage should be doubled until this rate of decline is
achieved.
 Decrease insulin infusion by 25-75% if the decline in serum
glucose is more than 100 mg/dL/h since this results in rapid

40. Sodium bicarbonate therapy
 Sodium bicarbonate therapy is generally not
indicated except for unstable patients with severe
acidosis such as an arterial pH < 6.9.
 Bicarbonate therapy is rarely indicated for HHS
patients
 NaHCO3 (50 mmol) is diluted in 200 mL sterile
water and infused at 200 mL/h.
 This may be repeated every 2 hours until the
venous pH is greater than 7.

41. Treatment of Precipitants
 Infection is the most common pathological
precipitant of DKA and HHS.
 The patient's entire skin surface should be
examined for wounds and cellulitis.
 Analysis and cultures of all appropriate body
fluids (blood, sputum, urine, cerebrospinal fluid)
should be obtained.
 The empiric administration of broad-spectrum
antibiotics should be considered until culture

42. Timeline for the typical adult patient with
suspected diabetic ketoacidosis.

43. Timeline for the typical adult patient with
suspected diabetic ketoacidosis.

44. Timeline for the typical adult patient with
suspected diabetic ketoacidosis

45. Complications Related to
Therapy
 Major complications related to therapy of DKA
include
 hypoglycemia
 hypokalemia,
 hypophosphatemia,
 adult respiratory distress syndrome
 cerebral edema.
 A gradual return to normal metabolic balance will
diminish the likelihood of such outcomes.

46. Complications, and Mortality

47. Cerebral edema
 occur in children, between 4 and 12 hours after the start of therapy,
or as late as 48 hours afterward.
 often seen when the patient appears to be improving clinically and
biochemically, and carries a high mortality.
 Subclinical brain swelling has been reported in asymptomatic
children during treatment of DKA.16
 There are no specific presentation or treatment variables that predict
or contribute to the development of cerebral edema.
 There is no evidence demonstrating an association between the
volume or sodium content of IV fluids or rate of change in serum
glucose and risk for cerebral edema.
 Gradual replacement of water and sodium deficits and slow
correction of hyperglycemia may lessen the risk.
 Young age and new-onset diabetes are the only identified potential
risk factors. Excessive initial fluid administration of >4 L/m2 of body
surface area per day has been associated with cerebral edema in

48. Disposition
 Patients with all but very mild cases of DKA and
all patients with HHS should have cardiac
monitoring and a higher level of nursing care for
at least 24 hours.
 Whether the patient goes to an intermediate care,
telemetry unit, or the intensive care unit is based
on severity of the case and response to initial
therapy as judged by the treating physician

49. THANK YOU