*Diabetic Coma
*Definition
*Diabetic coma is a life-threatening but reversible
form of coma found in people with diabetes mellitus.
*A diabetic coma results from either very high or very
low blood glucose levels.
*Diabetic coma is a dangerous condition that can lead
to unconsciousness and even death. Diabetic coma
may affect 2% to 15% of all diabetics at least once in
their lifetime.
*In most medical contexts, the term diabetic coma
refers to the diagnostically dilemma posed when a
physician is confronted with an unconscious patient
about whom nothing is known except that they have
*Types of Coma
*Three different types of diabetic coma
are identified:
[Link] Hypoglycaemia.
[Link] Diabetic Ketoacidosis.
[Link] Nonketotic Coma.
Sever
Hypoglycaemia
Definition
*Severe low blood sugar in a diabetic person
.
*People with type 1 diabetes mellitus who
must take insulin in full replacement doses
are most vulnerable to episodes
of hypoglycaemia (low blood glucose
levels).
Causes: (This can occur if)
1. Taking too much insulin or diabetic
medication.
2. Doing strenuous exercise without eating
additional food.
3. Missing meals.
4. Consuming too much alcohol, or
consumes alcohol without food.
Pathophysiology
*Hypoglycaemia occurs when the body has
insufficient glucose. If the brain does not
have enough glucose, it cannot function
properly which later cause death.
Clinical Picture
*Hypoglycaemia can be severe enough to cause
unconsciousness during sleep.
*Predisposing factors can include:
• Eating less than usual.
• Prolonged exercise earlier in the day.
*Unconsciousness due to hypoglycaemia can occur
within 20 minutes to an hour after early symptoms and
is not usually preceded by other illness or symptoms.
• Twitching or convulsions may occur.
• A person unconscious from hypoglycaemia is usually pale, has
a rapid heartbeat, and is soaked in sweat.
• The person is not usually dehydrated and breathing is normal
or shallow.
• Difficulty speaking.
• Blurry vision and confusion.
Investigations
*The blood sugar level, measured by a
glucose meter or laboratory measurement
at the time of discovery, is usually low but
not always severely.
Management
*It is usually mild enough to reverse by
eating or drinking carbohydrates, but blood
glucose occasionally can fall fast enough
and low enough to produce unconsciousness
before hypoglycaemia can be recognized
and reversed.
*Unconsciousness due to hypoglycaemia is
treated by raising the blood glucose by
administration of the hormone glucagon to
reverse the effects of insulin, or glucose
given intravenously.
Advanced Diabetic
Ketoacidosis
Definition
*Diabetic ketoacidosis (DKA) is a serious
complication of diabetes that can be life-
threatening. DKA is most common among people
with type 1 diabetes. People with type 2 diabetes
can also develop DKA.
*It results in unconsciousness from a combination
of a severely increased blood sugar level,
dehydration and shock, and exhaustion.
*Diabetic ketoacidosis (DKA) may occur at any
age.
Causes
*Very high blood sugar and low insulin levels lead to DKA.
The two most common causes are:
*Illness. When the patient get sick, he may not be able to
eat or drink as much as usual, which can make blood
sugar levels hard to manage.
*Missing insulin shots, a clogged insulin pump, or the
wrong insulin dose.
*Other causes of DKA include:
*Heart attack or stroke.
*Physical injury, such as from a car accident.
*Alcohol or drug use.
*Certain medicines, such as some diuretics (water pills) and
corticosteroids (used to treat inflammation in the body).
Pathophysiology
*Diabetic ketoacidosis (DKA), most typically
seen in those with type 1 diabetes, is
triggered by the build-up of chemicals called
ketones.
*DKA develops when the body doesn’t have
enough insulin to allow blood sugar into cells
for use as energy. Instead, the liver breaks
down fat for fuel, a process that produces
acids called ketones.
*When too many ketones are produced too
fast, they can build up to dangerous levels in
the body.
*These are strongly acidic and a build-up can
cause the blood to become acidic. When
these levels get too high it essentially
poisons the body and causes DKA.
*If it progresses and worsens without
treatment it can eventually cause
unconsciousness, from a combination of a
very high blood sugar level, dehydration and
shock, and exhaustion.
*Coma only occurs at an advanced stage,
usually after 36 hours or more of worsening
vomiting and hyperventilation.
Clinical Picture
* DKA usually develops slowly, early symptoms include:
• Being very thirsty.
• Urinating a lot more than usual.
* If untreated, more severe symptoms can appear quickly in the
early to middle stages of ketoacidosis, patients are typically:
• Fast, deep breathing.
• Visible dehydration: dry skin and mouth.
• Flushed face.
• Fruity-smelling breath.
• Headache.
• Muscle stiffness or aches.
• Being very tired.
• Nausea and vomiting.
• Stomach pain.
• Pale appearance from diminished perfusion.
• Fast heart rate is often present when coma is reached.
*If the patient is known to have diabetes, the diagnosis
of diabetic ketoacidosis is usually suspected from the
appearance and a history of 1–2 days of vomiting.
*Elevated ketones are a sign of DKA, which is a
medical emergency and needs to be treated
immediately.
*In case the patient is experiencing any of the
following:
• Blood sugar stays at 300 mg/dL or above.
• Breath smells fruity.
• Vomiting and can’t keep food or drinks down.
• Having trouble breathing.
• Multiple signs and symptoms of DKA.
*Sometimes DKA is the first sign of diabetes in people
who haven’t yet been diagnosed.
Investigations
*Laboratory Studies: Ketone testing may be
used in type 1 diabetes to screen for early
ketoacidosis. The ketone test is usually done
using a urine sample or a blood sample.
*Ketone testing is usually done when DKA is
suspected:
• Most often, urine testing is done first.
• If the urine is positive for ketones, most
often a ketone called beta-hydroxybutyrate
is measured in the blood. This is the most
common ketone measured. The other main
ketone is acetoacetate.
*Other tests for ketoacidosis include:
• Arterial blood gas
• Basic metabolic panel, (a group of blood tests that measure
your sodium and potassium levels, kidney function, and
other chemicals and functions, including the anion gap)
• Blood glucose test
• Blood pressure measurement
• Osmolality blood test
*The diagnosis is confirmed when the usual blood
chemistries in the emergency department reveal a high
blood sugar level and severe metabolic acidosis.
*Imaging studies: Radiologic studies that may
be helpful in patients with DKA include the
following:
• Chest radiography - To rule out pulmonary
infection such as pneumonia.
• Head computed tomography (CT) scanning
- To detect early cerebral oedema; use low
threshold in children with DKA and altered
mental status.
• Head magnetic resonance imaging (MRI)
- To detect early cerebral oedema (order
only if altered consciousness is present)
* Management
*The goal of treatment is to correct the high blood sugar
level with insulin. Another goal is to replace fluids and
bodily chemicals lost through urination, loss of
appetite, and vomiting if you have these symptoms.
*Treatment of diabetic ketoacidosis consists of:
• Replacing fluids: isotonic intravenous fluids to rapidly
stabilize the circulation.
• Replacing electrolytes: continued intravenous saline
with potassium, sodium and other electrolytes to
replace deficits.
• Receiving Insulin: insulin to reverse the ketoacidosis.
• Taking medicines: for any underlying illness that
caused DKA, such as antibiotics for an infection.
• Careful monitoring for complications.
*Pharmacotherapy: Medications used in the
management of DKA include the following:
• Rapid-acting insulins (eg, insulin aspart,
insulin glulisine)
• Short-acting insulins (eg, regular insulin)
• Electrolyte supplements (eg, potassium
chloride)
• Alkalinizing agents (eg, sodium
bicarbonate)
Hyperosmolar Nonketotic
Coma
Definition
*Coma occurs most often in patients who
have type 2 or steroid diabetes and have an
impaired ability to recognize thirst and drink.
*It is classically a nursing home condition but
can occur in all ages. It occurs predominantly
in subjects aged over 50 years.
Causes
*Hyperosmolar Hyperglycaemic coma usually occurs
in the at-risk population; it can also occur
spontaneously. The common predisposing factors of
nonketotic hyperglycaemia are:
• Inappropriate insulin dosing
• Serious systemic illness:
a. Advanced dehydration.
b. Severe acute metabolic stress (infection, inflammation, burns,
myocardial infarction, Cushing's syndrome).
c. Surgery or anaesthesia.
• Specific states of impaired carbohydrate tolerance (e.g.,
burns, drug therapy plus parenteral hyper-alimentation).
• Drug therapy that impairs fat mobilization in ketosis-
susceptible patients (e.g., propranolol therapy).
*In children and young adults with type 1 and type 2
diabetes, infectious diseases and disorders of the
respiratory, circulatory, and genitourinary systems
can cause Hyperglycaemic coma.
*Obesity and incessant consumption of carbohydrate-
rich beverages have led to an increase in the
incidence of Hyperglycaemic coma.
*A cardiovascular insult like stroke, angina pectoris,
and myocardial infarction can also trigger a stress
response. This leads to the release of counter
regulatory hormones with the resultant effect of an
increased level of blood glucose, causing osmotic
diuresis and dehydration, with the final result being
Hyperglycaemic coma.
Pathophysiology
*The pathophysiology of nonketotic
hyperglycaemic coma is similar to that of
diabetic ketoacidosis with one exception:
overproduction of acetoacetate and β-
hydroxybutyrate sufficient to cause ketoacidosis
does not occur.
*The basic bi-hormonal mechanism of uncontrolled
diabetes is no different: a relative or absolute
excess of glucagon. Elevation of the plasma
glucose level is, as in ketoacidosis, the result of
increased production of glucose by the liver
coupled with its diminished utilization in tissues.
*In hyperglycaemic coma, because insulin is still
being produced by the beta cells in the pancreas,
the generation of ketone bodies is minimal. Insulin
inhibits ketogenesis. That aside, in hyperglycaemic
coma, there is a higher level of insulin with an
associated lower level of glucagon. Therefore,
ketonemia and acidemia, if they happen, they are
very mild in hyperglycaemic coma.
*Nonketotic hyperosmolar coma usually develops
more insidiously than diabetic ketoacidosis because
the principal symptom is lethargy progressing to
obtundation, rather than vomiting and an obvious
illness.
*Coma usually occurs in patients with type 2 in
which an extremely high blood sugar level and
dehydration alone are sufficient to cause
unconsciousness.
Clinical Picture
*Extremely high blood sugar levels are
accompanied by dehydration due to
inadequate fluid intake.
*Thediagnosis is usually discovered when a
chemistry screen performed because of
obtundation reveals an extremely high
blood sugar level (often above 1800 mg/dl
(100 mM)) and dehydration.
*If an infectious process precedes hyperglycaemic
syndrome, signs and symptoms include:
• Fever
• Malaise
• General weakness
• Tachypnoea
• Tachycardia
*If the precipitating factor is a cardiac or vascular
condition, signs and symptoms will include:
• Chest pain
• Chest tightness
• Headache
• Dizziness
• Palpitations
*The typical clinical presentation of patients
with hyperglycaemic syndrome is increased
urination (polyuria) and increased water
intake (polydipsia). This is a result of the
stimulation of the thirst centre in the brain
from severe dehydration and increased
serum osmolality.
*Weakness, malaise, and lethargy can also be
part of the complaints.
*Severe dehydration from hyperglycaemic
syndrome can also affect the skin and
integumentary system. Typically, the skin and
the oral mucosa are dry with a delayed
Investigations
*The evaluation of hyperglycaemic syndrome
requires a detailed history and physical
examination.
*The onset of symptoms and the precipitating
factors are very important to elicit from
patients.
*The first test in hyperglycaemic syndrome is
a finger stick to determine the serum glucose
level. The value is usually between 600 to
1200 mg/dl. The higher the level of glucose,
the greater the serum osmolarity and the
higher the degree of dehydration.
*Glucose: The glucose level should be
monitored hourly to guard against a sudden
and precipitous drop during treatment with
isotonic fluid and insulin.
*Haemoglobin A1C: This is a measure of long-
term glycaemic control and is a useful tool in
the assessment of new-onset diabetes
mellitus.
*Sodium: The sodium level is falsely low.
*Serum Osmolarity: The serum osmolality is very
high in hyperglycaemic syndrome.
• Levels between 320 to 400mOsm/kg are very common.
• Normal serum osmolarity is around 280 -290 mOsm/kg.
• Higher serum osmolarity is associated with alteration
in the level of consciousness and might eventually lead
to a coma.
*Potassium: The level of potassium might be high
or low.
* A low level of insulin can cause an extracellular shift of
potassium.
*Bicarbonate: Bicarbonate level is usually close to
normal in hyperglycaemic syndrome, around 8 to 12
mmol/L, because the production of ketone bodies is
minimal as compared to DKA, where the bicarbonate
level is usually very low.
*Magnesium: The magnesium level might be
low in hyperglycaemic syndrome.
*Ketones: Ketonemia is very minimal in
hyperglycaemic syndrome. Electrolytes
should be monitored serially every 2 to 3
hours in the management plan.
*Arterial Blood Gases
• The role of blood gas is to determine the level of
acidosis.
• In hyperglycaemic syndrome, pH is usually above
or around 7.30.
• The pC0 might be low from hyperventilation.
• Arterial blood gases should be monitored every 2
to 3 hours.
*Renal Function
* The BUN and creatine levels are usually elevated, reflecting pre-
renal azotemia.
* As hydration and insulin therapy are initiated, these values will
usually drop and eventually normalize.
*Serum Enzymes
* The level of serum enzymes like creatinine kinase, aldolase, and
transaminases is usually high from hemoconcentration and
dehydration.
*Complete Blood Count
* The white blood cell count might be high because of the stress
response or as a result of an infectious process triggering
hyperglycaemic syndrome.
* In most cases, haemoglobin and haematocrit levels are elevated.
* If the white count is elevated, blood culture, urine culture, and a
chest X-ray might be needed to find the source of infection.
*Urine Analysis
* Urine-specific gravity is high in HHS. Glycosuria and ketonuria are
also present.
Management
*Appropriate resuscitation with attention to the principle of
Airway, Breathing, and Circulation (ABC) should be
initiated.
*treatment consists of:
• Given Insulin.
• Gradual rehydration with intravenous fluids.
• Potassium and sodium given as soon as possible.
*Immediate Management of Hyperglycaemic Comas:
• Be aware of hyperglycaemic coma as a possibility.
• Test for hyperglycaemia, ketosis, and acidosis.
• Screen for any precipitating illness (e.g., infection,
cerebral or myocardial infarction, inadequate
treatment).
• Institute a slow insulin infusion guided by frequent
bedside blood glucose monitoring to halve
glucose level over 4 hours.
• Arrange prompt, adequate fluid replacement with
0.9% saline (if Na less than 155 mmol/L) or 0.45%
saline (if Na greater than 155 mmol/L) at 500 mL/hr
over first 4 hours.
*In paediatrics, rehydration and electrolyte correction
over a longer period of 48 hours may help in the
prevention of cerebral oedema.
