Acute diabetes complications

DKA and HHS

Diabetic ketoacidosis (DKA)
Diabetic ketoacidosis (DKA) is a cardinal feature of type 1 diabetes.
However, it is rare for DKA to occur in type 2 diabetes in the absence of
some precipitating event.
When DKA occurs in an individual with type 2 diabetes, the clinician
should look under the sheets and initiate an intensive search for the
precipitating factor
DKA
A triad of :
Uncontrolled hyperglycemia
Increased total body ketone concentration
Metabolic acidosis (High anion gap)
due to
Absolute insulin deficiency
Pathogenesis
These metabolic derangements result from the combination of
absolute or relative insulin deficiency and an increase in counter
regulatory hormones
glucagon.
.catecholamines
cortisol.
.growth hormone
Pathogenesis of DKA
Absolute insulin deficiency Hyperglycemia and Intracellular starvation
Counterregulatory hormone response (stress response) ;
1-Gluconeogenesis
Breakdown of protein and conversion of amino acids into glucose.
2-Glycogenolysis
Breakdown of liver glycogen into glucose
3-Lipolysis
Ketogenesis (Hepatic fatty acid oxidation) and formation of Ketone bodies
(betahydroxybutyrate and acetoacetate,acetone) that are acids
(H+/anions) build up in the blood stream (increase in anion gap)
Ketonemia and metabolic acidosis
DKA
precipitating factor:
1. Infections (the most common): Chest infections , UTI
2. Stress of illness such as:
Trauma
Surgery
Myocardial infarction
Cerebrovascular stoke
 3. Discontinuation of or inadequate insulin therapy

DKA- Clinical presentation

Symptoms
A. Hyperglycemia
1. Polyuria
2. Polydipsia
3. Non-specific
4. Weakness
5. Lethargy
6. Myalgia
7. Headache
B. Gastrointestinal
1. Anorexia
2. Nausea
3. Vomiting
4. Abdominal pain
C. Respiratory : Dyspnea
Signs
1. Hypotension & tachycardia
2. Kussmaul respiration
3. Acetone breath
4. Dehydration
5. Tender abdomen
6. Stupor up to coma
7. Focal neurological signs (hemiparesis, aphasia, seizeres..etc)
especially in HHS

DIABETIC KETOACIDOSIS (DKA)

Laboratory investigations
Hyperglycemia
Blood glucose >250 mg/dL
Ketonemia
Serum ketones positive
High anion gap metabolic acidosis
pH < 7.30
HCO3- < 15 mEq/L
Metabolic Acidosis With Increased Anion Gap
(Anion gap = No of anions No of cations)
AG = [ Na+] [ Cl - + HCO3 - ]
N 7-9 mEq/L
In a typical case of DKA, the AG is > 10 mEq/L
Mild to moderate DKA ( can be managed in the ward) but severe DKA
should be managed in ICU.

Criteria of severe DKA:

PH< 7
HCO3< 10mEq/L
Ketone body positive
Anion gap > 12
Stupor or coma
Differential diagnosis of DKA
Hyperglycemic Hyperosmolar State ( HHS)
HHS is characterized by :
severe hyperglycemia,
hyperosmolality, and dehydration
in the absence of significant ketosis due to Relative insulin deficiency

HHS
The relative insulin deficiency is inadequate to prevent
hyperglycemia (Gluconeogenesis & Glycogenolysis) but adequate to
prevent lipolysis and subsequent
Ketogenesis.

Precipitating Factors
HHS
1.Infection is the most common precipitant cause
2.Restricted water intake that likely result in severe dehydration.
This is due to:
the patient being bedridden .
the altered thirst response of the elderly.
3.Delayed recognition of hyperglycemic symptoms (20% of these
patients have no history of diabetes)
HHS /Clinical presentation

HHS is similar to DKA except ketosis is absent or minimal Ketosis.

Absence of ketosis and acidosis delay
seeking medical advice and therefore the patient presents with
marked
hyperglycemia and dehydration

Therefore patients with HHS compared to those with DKA have:

marked manifestations of dehydration less GI symptoms
No Kussmaul respiration and no Acetone breath.
Menal status is more affected (altered level of consciousness due to
hyperosmolarity) , focal neurological deficits (hemianopia and
hemiparesis) and seizures (focal or generalized) are more common.

HHS
Laboratory Diagnosis
Plasma glucose >600 mg/dl
Effective serum osmolality > 320 mOsm/kg
Arterial pH >7.3 , HCO3> 15 mEq/l
Absence of significant ketoacidosis (minimal or no ketosis)
Effective serum osmolality =

Treatment Objectives
Improve circulatory volume and perfusion
Correct electrolyte disturbances
Provide adequate insulin to restore and maintain normal glucose
metabolism and correct acidosis
Prevent complications resulting from treatment
Identification of precipitating conditions
Provide patient and family education and follow-up
I. Fluid Therapy
First line.
The aim is to correct ( intravascular , interstitial and intracellular)
volume depletion, hypertonicity and renal perfusion.
It usually started before insulin therapy especially in patients with
severe volume contraction and hypokalemia.
Type of fluid :0.9% NaCl
1 Liter of 0.9% NaCl per hour to avoid overcorrection that may lead to
cerebral edema.
II. Insulin Therapy
Insulin therapy is a cornerstone in management
The aim of insulin therapy is to correct hyperglycemia (6 h) and
reverse ketoacidosis (metabolic acidosis) (12 h)
Regular insulin can be administered via continuous intavenous
infusion protocol.
It is preferable to postpone insulin therapy until the results of
serum potassium are obtained
Insulin should not be given if hypokalemia or severe volume
contraction is present unless these conditions are corrected
Management of DKA
During treatment of DKA, hyperglycemia is corrected faster (~6
h) than ketoacidosis(~12h).

When serum glucose reaches 200 mg/dl in DKA 5% dextrose

should be added to allow continued insulin administration until
ketonemia is controlled while at the same time avoiding
hypoglycemia.

III. Potassium Therapy

Mild-to-moderate hyperkalemia at presentation is usually corrected by
insulin therapy, correction of acidosis, and volume expansion.
To prevent hypokalemia, potassium replacement is initiated when serum
level is less than 5.2 mEq/l.
The treatment goal is to maintain serum potassium levels within the
normal range of 45 mEq/l.
(2030 mEq potassium in each liter of infusion fluid)
III. Potassium Therapy
If serum K is less than 3.3 mEq/l , hold insulin treatment until
serum K is
restored to 3.3 mEq/l to avoid life-threatening arrhythmias and
respiratory muscle weakness.

IV. Bicarbonate Therapy

The use of bicarbonate in DKA is controversial because most experts
believe that during the treatment, as ketone bodies decrease there will
be adequate bicarbonate except in severely acidotic patients.
So , the use of bicarbonate therapy is only indicated in severe
metbolic acidosis (pH is < 6.9 )
The treatment goal is to maintain the pH 7

Side effects of bicarbonate therapy

Hypokalemia
Overshoot alkalosis
Therefore the use of bicarbonate therapy is only indicated in
severe acidosis (pH is < 6.9)

Criteria for DKA resolution

Criteria for resolution of ketoacidosis:
blood glucose < 200 mg/dl and two of the following criteria:
1-a serum bicarbonate level 15mEq/l
2- a venous pH > 7.3
3- and a calculated anion gap 12 mEq/l.
Criteria for resolution of HHS:
normal osmolality and regain of normal mental status.
blood glucose < 300 mg/dl
Criteria for resolution
Monitoring of plasma ketones is not practical and monitoring
urine acetone is misleading
Monitoring of DKA

-OHB direct measurement in the blood is the preferred method for

monitoring DKA but it is not practical.
-OHB is the strongest , predominant and most prevalent acid in
DKA.
-OHB is not measured by the nitroprusside method (measures only
acetoacetic acid and acetone in blood and urine)
False results of urine tests of Ketones
Most urine testing kits detect aceto-acetate only, not the predominant
ketone -OHB.
It is possible for the test to be false negative with high levels of beta-
hydroxybutyrate.
It is possible for the test to be false positive : During therapy, -OHB is
converted to acetoacetic acid so the urine test becomes positive (to
aceto-acetate).

Therefore, assessments of urinary ketone levels should not be

used as an indicator of response to therapy

VII. Transition to
subcutaneous insulin
To prevent recurrence of hyperglycemia or ketoacidosis during the
transition period to Sc insulin, stop IV insulin 1-2 h after the first SC
dose due to very short half life of IV insulin.
Patients with known diabetes may be given insulin at the dosage they
were receiving before the onset of DKA so long as it was controlling
glucose properly.
In insulin-nave patients, a multidose insulin regimen should be started
at a dose of 0.5 0.8 units/kg/day by using either the conventional or
Basal/Bolus regimens. Both regimens have similar glycemic control
during transition. However, treatment with basal bolus is associated with
lower rate of hypoglycemic events.
Complications of DKA treatment
Hypoglycemia and hypokalemia are two common complications with
overzealous treatment of DKA with insulin and bicarbonate
respectively.
Cerebral edema during treatment, esp in children ,presented by onset of
headache, gradual deterioration in level of consciousness,
seizures, sphincter incontinence, pupillary changes, papilledema,
bradycardia, elevation in blood pressure, and respiratory arrest

Mechanisms of cerebral edema include:

A rapid fluid shift from extracellular to intracellular by rapid

correction of
osmolality and dehydration

Prevention of cerebral edema

Prevention might include
1-Avoidance of excessive hydration.
2- Avoidance of Rapid reduction of plasma osmolarity.
3-Gradual decrease in serum glucose.

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