Disorders of Carbohydrate Metabolism.

ABDELMONIEM SAEED MOHAMMED

ER SPECIALIST
Disorders of Carbohydrate Metabolism.

 INCLUDES
 Diabetic ketoacidosis
 Hyperosmolar Hyperglycemic state(HHS)
 Hyperglycemia
 Hypoglycemia
 Lactic acidosis
 Alcoholic ketoacidosis
Most CH metabolism disorders r 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.
 Diabetic ketoacidosis

Most common acute life threatening complication of

Diabetes.
Commonly type 1 DM, may occur in type 2
pathophysiology
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

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
CLINICAL FINDINGS
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 confusion to coma

Investigation
Routine lab
CBC
RFT
RBG
UG
ABG

Radiological imaging
CXR

Other
ECG
Coagulation profile
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.
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.
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
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,
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 replacement.
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

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.
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
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
HYPEROSMOLAR HYPERGLYCEMIC STATE
(HHS)
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
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.
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
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.

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);
Laboratory Findings

Key laboratory findings—Key findings to diagnose

HHS and differentiate it from DKA are as follows:
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.
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.
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.
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
Treatment
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
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
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 0.9% NaCl

solution to restore blood pressure to at least 90 mm Hg.
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 more than ~3
mOsm/kg/h due to increased risk of cerebral edema.
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.
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 mEq/L below normal
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 shifts in serum osmolality.
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.
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 results are available.
Timeline for the typical adult patient with
suspected diabetic ketoacidosis.
Timeline for the typical adult patient with
suspected diabetic ketoacidosis.
Timeline for the typical adult patient with
suspected diabetic ketoacidosis
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.
Complications, and Mortality
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 some studies
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
THANK YOU