Diagnosis & ManagementDr.

Ahmados
of diabetic
patient

1- Diabetic Ketoacidosis (DKA)

General Considerations :
-It is more commonly seen in type 1 diabetes but may
occur in type 2.
-When the production of insulin in the pancreas fails, the
decreased glucose utilization creates a relative state of
starvation.
-Counter regulatory hormones (cortisol, glucagon,
catecholamine, and growth hormone) that help maintain
blood glucose levels adequate for cellular function
during fasting are stimulated  which promote
gluconeogenesis & glycogenolysis, increasing glucose
levels, and lipolysis, which converts adipose to free
fatty acids.
-Without insulin to allow cellular utilization of glucose,
these mechanisms continue to produce glucose.
-Severe dehydration and electrolyte losses develop as
the kidneys filter the highly osmotic glucose.
- Free fatty acids that cannot enter the citric acid cycle
without insulin are oxidized into ketones. These
accumulate to cause metabolic acidosis & further
electrolyte derangement.
Causes : ( 4 I ): If a diabetes history is known, potential
precipitating causes of DKA:
1- Infection: recent or current, Chest ( ask about
cough, sputum) – Skin ( ask about itching , skin colour
change ) – ………………
…….Genitourinary (ask about vaginal discharge,
dysuria , frequent macturation )
…………………………………GIT
( Gastroenteritis ).
2- Infarction: Heart (ACS or myocardial infarction)
- Pulmonary ( pulmonary embolism) - Brain
(TIA or Stroke) .
3- Insulin insufficient: Normal insulin administration
is up to 40 IU/day .
4- Intercurrent illness .
Others :
-Injury or trauma
-Medications (corticosteroids, thiazides, or
sympathomimetics)
-Ethanol or drug abuse
-Psychosocial factors, such as depression or
inability to afford medications, limiting
compliance.
Symptoms & signs include: A fruity or acetone-like
odor is classically described along with :
1- Polyuria , Polydepsia , Polyphagia .
2- Nausea & Vomiting. (Emesis may have a
coffee ground appearance due to hemorrhagic
gastritis)
3- Fatigue,
4- Altered mental status (changes ranging from
mild confusion to coma )
5- Tachypnea (Kussmaul's respirations) rapid
deep respirations attempting to compensate for
acidosis.
6- Tachycardia,
7- Abdominal pain .

Diagnosis: ( D – K – A ): there is a history of

precipitating factors (see above)
- Diabetic  Random blood sugar is high.
- Keton bodies  Urine analysis shows keton
bodies.
- Acidosis  ABG shows acidosis. (Normally: pH
7.35 – 7.45) ( DKA: pH < 7.3 AND serum HCO3
<=15 mEq/L )
Other Laboratory Findings : Dr.Ahmados

Serum Serum Sodium Serum Phosphate

Potassium
Acidosis drives Diuresis & May be normal or
potassium out of vomiting   elevated despite
the cells  serum Na deficits
causing a  approaching 1
serum k despite mmol/kg body
Osmotic pressure
total body weight.
from glucose also
deficits.
 dilutes the serum
If serum lowers Na . Routine phosphate
potassium is repletion does not
Correction :
initially low, improve outcome
This effect can be
insulin in DKA and is
corrected by
administration generally not
adding 1.8
will exacerbate indicated in the
mEq/L to the
the situation by emergency
serum sodium
facilitating the department.
concentration for
cellular entry of
each 100 mg/dL Severe
potassium.
above normal. hypophosphatemia
Severe (<1 mg/dL),
N.B. rapid
hypokalemia however, may
correction with
may cause : cause skeletal,
increasing
cardiac, and
1- fatigue osmolality may
respiratory muscle
2- muscle precipitate
depression.
cramps cerebral edema,
Phosphate should
especially in
3- lethal be replaced in this
children.
arrhythmia. circumstance.
Correction :
This can be done
by using potassium
phosphate as 1/3 of
potassium
replacement.
 Serum Osmolality (N
Anion Gap
285 mOsm/kg)
The anion gap is useful to -Serum osmolality value
assess severity of acidosis above 340 mOsm/kg
and to follow progress of usually result in menta
therapy. The anion gap is status changes (letharg
obtained from the formula: or coma)
-Below this value, other
Anion gab = (Na) – (Cl) +
causes for lethargy or
(HCO3) .
coma should be
Normal values are : 8 - 16. investigated.
-This value may also be
used to diagnose
hyperosmolar
hyperglycemic state
(HHS)
Effective serum
osmolality can be
estimated by formula:
Serum Osmolality /litre
2 [Na+ + K+] + glucose
(mmol/litre) + urea
(mmol/litre)

Serum Ketones ( reading ) :

- Not always reliable as a diagnostic test.
- The primary ketone body formed in DKA initially is B-
hydroxybutyrate. However, standard ketone assays
measure only acetoacetate. Since insulin is required for
the conversion of B-hydroxybutyrate to acetoacetate
these assays may be reassuringly negative even in a
severely ill patient.

Summary of investigation
Aim to both confirm the diagnosis and search for

Blood Urea Nitrogen possible underlying cause(s):

 Urine analysis for glucose and ketones and
 Send blood sample for Glucose, U&E (urea &
Creatinine electrolytes),
…………………………………………. .Creatinine,
Osmolality .
 Check ABG ( for metabolic acidosis ± respiratory
These levels may be compensation )
 Calculate the anion gap (normal should be 14-
elevated  because 18mmol/L.) A normal anion gap makes DKA
unlikely. of :
1- severe  CBC.
 CXR (to search for pneumonia)
dehydration,  ECG and cardiac monitoring (look for evidence
of hyper-/hypokalaemia)
2- acute  Blood cultures & if appropriate, throat or wound
swabs
tubular
necrosis, or renal
failure.

Treatment: ( Below )

2- Hyperosmolar Hyperglycemic Non-Ketotic state

Essentials of diagnosis
(HHNK)
-Most symptoms relate to severe dehydration
 -Absence of acidosis + small or absent serum
ketones + hyperglycemia usually 600 mg/dL
-Kussmaul's respirations & abdominal pain are
Dr.Ahmados
unusual findings
General Considerations
-In contrast to DKA, patients with HHNK have
sufficient insulin activity to prevent lipolysis and
ketogenesis.
-HHS results from gradual diuresis, resulting in  1)
severe dehydration & 2) electrolyte depletion,
without significant early symptoms (DKA often
manifests symptoms more suddenly over hours to a
few days due to acidosis.)
-This leads to profound electrolyte deficiencies &
eventually mental status changes.
Causes :
HHS is most commonly seen in older patients
( diabetes type II ) and is often caused by physiologic
stressors such as infection, myocardial infarction,
cerebrovascular accident, trauma, decreased access to
water, and drug effects or interactions.
Clinical features :
History :
Presentations is a patient 65 or more years old
with : long period of starvation, dehydration,
 with history of precipitating factors as change in
diabetes regimen, addition of medications that may
elevate glucose levels (e.g., corticosteroids,
thiazides, anticonvulsants, sympathomimetics),
recent or current infection.
Symptoms & Signs :
-These include Polydipsia, Polyuria, or Polyphagia .
-Fatigue
-Altered mental status (clouded thinking to
confusion to lethargy or coma);
-Signs: dry mucous membranes; poor skin turgor;
and delayed capillary refill.
N.B.
- Abdominal pain is not a typical finding in HHNK (in
contrast to DKA);
- Acute cholecystitis & appendicitis may be insidious
and have an atypical presentation in elderly patients.
 Serum Serum
Diagnosis: Potassium Sodium
Key findings to diagnose Serum In the early
HHNK and differentiate it potassium stages of
from DKA are as follows: levels will HHNK, serum
most sodium
1- Serum glucose  600
commonly findings are
mg/dL. be normal similar to
2- Urine analysis  ketones
or low, those in
are absent or small (2ry to unless patients with
starvation) … renal DKA.
……Glucosuria is failure is
prominent. Urinary losses
present.
3- Serum osmolality is and fluid
Total.
320 mOsm/kg. shifts out of
4- pH is usually > 7.30. the cell and
Total body
5- Serum bicarbonate is into the
deficits
usually > 15 mEq/L. extracellular
are often
6- The anion gap may be 4 - 6 compartment
variable depending on create
mEq/L or
precipitating cause but is hyponatremia
as much as
usually 10. usually 125-
500 mEq
130 mg/dL.
Blood Urea Nitrogen and total.
Creatinine Correction :
Correction for
-Blood urea nitrogen (BUN) hyperglycemia
is often markedly elevated with the
 . addition of 1.8
-Gastrointestinal bleeding mg/dL sodium
may also elevate BUN and is per 100 mg/dL
 a possible precipitating cause of HHS in elderly
patients.
Dr.Ahmados
Treatment of DKA & HHNK is similar

Monitoring: Continuous monitoring of vital signs,

mental status, and laboratory parameters is essential.
1) Resuscitation issues
- If altered consciousness/coma is present, provide and
maintain a patent airway.
- Oxygen therapy is indicated for all DKA or HHNK
patients, and maintaining oxygen saturation above
96% or PO2 70 mm Hg.
2) Fluid therapy
( Overall fluid deficits approach 6-10 L in most
patients )
- Intravenous lines are essential. Central venous access
may be indicated.
- Usually 1 - 1.5 L of 0.9% saline ( if the lab result
subsequently shows initial plasma Na+ to be
>150mmol/litre, give 0.45% saline ) is infused
over the first hour  Subsequent infusion can be
decreased to 500 mL/h, then 250-500 mL/h, then 150-
300 mL/h as the hydration status improves.
- Hypotension should prompt a bolus of 1-2 L of 0.9%
NaCl solution to restore blood pressure to at least 90
mm Hg.
N.B.
- 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.

- The calculated serum osmolality should not decrease

more than ~3 mOsm/kg/h due to increased risk of
cerebral edema.
3) Insulin therapy
- Intravenous regular insulin (short acting) is used for
initial therapy. Then :
- A continuous infusion of regular insulin at 0.1
Unit/kg/h is the treatment of choice.

Then, measure the RBG each hour :

- If glucose is not decreasing by 50 - 70 mg/dL/h  the

insulin dosage should be doubled until this rate of
decline is achieved.
- If the decline in serum glucose is more than 100
mg/dL/h  decrease insulin infusion by 25 - 75%

N.B.
Insulin therapy should be delayed if the potassium level
is less than 3.3 mEq/L until the potassium level is rising.
4- Potassium replacement ( K )
-Potassium replacement with target levels of 4.0 - 5.0
mEq/L .

If serum K is 3.3 mEq/L or less,

1- give 40 mEq potassium chloride IV or
2- a mixture of 2/3 potassium chloride & 1/3
potassium phosphate (~5 mmol) if serum phosphate
is less than 1 mmol/L.

If serum K is 3.3-5.0 mEq/L, give 20-30 mEq KCl in

each liter of intravenous fluid.

If serum K is 5.0 mEq/L or more, hold potassium

repletion & 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.
5- Antibiotics
-Infection is the most common pathological precipitant
of DKA and HHS.
-Analysis and cultures of all appropriate body fluids
(blood, sputum, urine, cerebrospinal fluid) should be
obtained.
-The empirical administration of broad-spectrum
antibiotics ( 3rd generation cephalosporin) until culture
results are available.
Treatment of HHNK is similar to DKA + Prophylactic
anticoagulant ( prophylactic against embolism which
may leads to cerebrovascular stroke )

3- Hyperglycemia
Patients with either known or undiagnosed diabetes may
present with symptoms due to hyperglycemia,
complications of untreated diabetes,
Causes : Missed dose + Over eating + (4 I):
1- Infection: recent or current, Chest ( ask about
cough, sputum) – Skin ( ask about itching , skin colour
change ) – ………………
…….Genitourinary (ask about vaginal discharge,
dysuria , frequent macturation )
…………………………………GIT
( Gastroenteritis ).
2- Infarction: Heart (ACS or myocardial infarction)
- Pulmonary ( pulmonary embolism) - Brain
(TIA or Stroke) .
3- Insulin insufficient: Normal insulin administration
is up to 40 IU/day .
4- Intercurrent illness .
Dr.Ahmados
Clinical features :
History
-Age greater than 45, obesity, physical inactivity, and
family history are risk factors for insulin resistance.
-Personal history of gestational diabetes, impaired
glucose tolerance, hypertension, dyslipidemia,
vascular disease, or polycystic ovary disease also
increases risk.
Symptoms & Signs :
-polydipsia, polyuria, polyphagia,
-weakness, fatigue,
-Neurological manifestations: headache, blurred
vision, dizziness, all grades of coma.
-dehydration
Laboratory Findings : ( for diagnosis & cause )
-A random serum glucose > 200 mg/dL + symptoms
of hyperglycemia
-2h postprandial > 180 mg/dl
-Fasting serum glucose > 126 mg/dL
-Glycosylated hemoglobin ( HgA1C ) >= 7% .

-Severe hyperglycemia (>=400 mg/dL) may

foreshadow impending decompensation.
 An underlying cause should be sought aggressively
such as infection, cardiac ischemia, or myocardial
infarction. White blood cell count, blood cultures,
and ECG with cardiac enzymes may be helpful.
Treatment
1- If diabetes was previously undiagnosed &
insulin deficiency (type 1) cannot be excluded,
then the patient should be admitted.
2- If hyperglycemia is mild (<250 - 350 mg/dL)
with no signs of decompensation, no specific
treatment is required if primary care follow-
up** is readily available.
3- If the serum glucose is greater than 300
mg/dL, treatment is as follows:
Fluids
Normal saline 1 L given over 1 hour, may be
adequate monotherapy for hyperglycemia.
Insulin
Usually 0.1 - 0.15 Unit/kg regular insulin, insulin
lispro (Humalog), or insulin aspart (NovoLog)
subcutaneously or intravenously can be given.
Oral Hypoglycemic Agents
-Not indicated for acute therapy of severe
hyperglycemia.
 -It can be initiated or continued by emergency
physicians when follow-up is available.
** Follow up : 1- Readjustment of the drugs (Oral
agents  insulin)
……………………2- Diet control
……………………3- Treatment of the cause ( infection
 antibiotics )

Disposition
Most patients with blood glucose less than 250�€“ 350
mg/dL in the absence of metabolic decompensation can
be safely discharged with follow-up after a thorough
evaluation for underlying illness. Patients with serious
underlying precipitants or in whom hyperglycemia is
resistant to treatment should be hospitalized.

4- HypoglycemiaDr.Ahmados
Essentials of Diagnosis
 Autonomic Manifestations are common and
include: diaphoresis, hunger pain, tremors ,
tachycardia , irritability, related to increased
circulating catecholamines ( No autonomic
manifestations in hyperglycemia )
 Neuroglycopenic Manifistations as
hypoglycemia progresses range : confusion or bizarre
behavior, lethargy, or coma
 Always check the fingerstick blood glucose on
every patient presenting with altered mental status or
who appears to be acutely ill
Causes :

- If low blood level < 45 mg/dl  Ask the patient if he

diabetic or not :

a- If the patient is know diabetic , the possible

causes are :
1. Diabetic nephropathy, ( no excretion of
insulin  increase insulin effect ) ,, most
important cause 40%.
Diagnosis of diabetic
nephropathy:
1- Serum creatinine
2- Urine analysis 
proteinuria
3- U/S  atrophic kidney
2. Insulin or oral agents overdose .
3. Delay in eating after taking insulin,
general malnutrition, or inadequate caloric
intake due to nausea and vomiting or
gastroparesis
4. Increased physical activity
 5. Increased physiologic stress resulting from
infection or injury
6. Excessive insulin release produced by
sulfonylurea drugs, especially in the presence
of renal insufficiency

a- If the patient is not diabetic , the possible

causes are : ( EXPLAIN )
1- Exogenous drugs (Intentional hypoglycemia
** C-peptide is naturally secreted along with

by insulin, or oral hypoglycemic agents taken by

insulin by the pancreas and is not present in
manufactured insulin. High insulin level
without a correspondingly high C-peptide

patients) **
level is diagnostic of exogenous insulin.

2- Pituitary insufficency (no GH or cortisol)

3- Liver failure (no glycogen stores)
4- Adrenal failure (no cortisol)
5- Insulinomas/ Immune hypoglycemia
6- Non-pancreatic neoplasms (retroperitoneal
sarcoma)
Others:
7- Pancreatic B-Cell Tumor :
Tumor of the insulin-secreting B-cells in the
islets of Langerhans may cause refractory
hypoglycemia and even coma. C-peptide levels
will elevate concurrently with insulin levels.
8-Excessive ethanol intake, especially without
adequate caloric intake, may cause severe
hypoglycemia (especially in children).
 9- Postprandial or Reactive Hypoglycemia :
The intake of large amounts of concentrated
calories in nondiabetics may produce enough
excess insulin to induce mildly symptomatic
hypoglycemia. Rarely, hypoglycemia may be
severe enough to cause briefly decreased level
of consciousness.
Clinical features :
History ( from the patient or the family )
-The patient is diabetic or not ?!
-History of alcohol use, recent caloric intake,
alterations of medication regimen, and recent
illness or injury.
Symptoms & Signs
-Autonomic manifestations:
Most early symptoms & signs are the result of
increased catecholamine release: tachycardia,
irritability, diaphoresis, paresthesias, hunger, and
decreased concentration are common.
-Neurological Manifestations:
With more severe or prolonged hypoglycemia,
symptoms and signs of neuroglycopenia result in
mental status changes including confusion or
bizarre behavior, lethargy, or coma; visual
disturbances such as blurred vision, diplopia,
hallucinations; seizures or seizure-like activity or
 focal neurologic deficits similar to Todd's paralysis
that resolves with glucose administration.
Dr.Ahmados
Laboratory Findings : ( for diagnosis & cause )
Diagnosis : Fingerstick glucose is a rapid screen to
determine blood glucose levels < 45 mg/dl .
Search for ancillary causes of hypoglycemia .

Treatment : Check random blood sugar : If low

blood level < 45 mg/dl  Ask the patient if he diabetic
or not !
- Emergency Therapeutic Measures :
1) Intravenous Glucose : ( small high concentrated
glucose )
If intravenous access is available, administer 50 cc
of 50% dextrose in water (containing approximately
25 g of glucose, which is enough to resolve most
hypoglycemic episodes)  Repeat dosages of 50%
dextrose may be necessary to maintain adequate
blood glucose levels.
Caution: Remember to give thiamine, 100 mg
intravenously or intramuscularly, to alcoholic
patients to prevent Wernicke's encephalopathy.
 Monitor the patient's mental status and recheck
capillary blood glucose 15 - 30 minutes after glucose
administration.
N.B.
1- Neurological manifestations may take time to
resolve completely.
2- If abnormalities persist longer than 30 minutes
after glucose administration & hypoglycemia has not
recurred, other causes should be investigated ….with
a cranial CT scan and appropriate laboratory studies .
2) Glucagon :
If intravenous access is not readily available, 1 mg
of glucagon may be given IM. The response time is
typically 10 - 15 minutes,
Side effects: nausea & vomiting along with
overcorrection of glucose levels are common.

3) Oral Feeding :
As soon as the patient regains consciousness :
- clear fruit juice (e.g., apple, grape; 6 oz = ~15 g
glucose) is a good choice to maintain glucose levels,
- a snack or meal is appropriate.
Monitoring
Hourly capillary glucose checks should be taken until
glucose levels are stable.

N.B.
The persistence of an altered conscious level suggests
another underlying pathology (eg CVA), or may reflect
the development of cerebral oedema due to
hypoglycaemia, which has a high mortality

Dr.Ahmados Source :
Current Emergency Diagnosis & Treatment - 6th Ed