DIABETIC COMA

KABERA René,MD
PGY III Resident
Family and Community Medicine
National University of Rwanda
PLAN
• Introduction
• Hypoglycemic coma
• Hyperglycemic coma

Diabetic Ketoacidosis

Hyperglycemic hyperosmolar state

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INTRODUCTION
• Diabetes mellitus (DM) refers to a group of common metabolic disorders that
share the phenotype of hyperglycemia.
• Several distinct types of DM exist and are caused by a complex interaction of
genetics and environmental factors.
• Depending on the etiology of the DM, factors contributing to hyperglycemia
include reduced insulin secretion, decreased glucose utilization, and
increased glucose production.

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INTRODUCTION
• The metabolic dysregulation associated with DM causes secondary
pathophysiologic changes in multiple organ systems that impose a
tremendous burden on the individual with diabetes and on the health care
system.
• DM is the leading cause of end-stage renal disease (ESRD), nontraumatic
lower extremity amputations, and adult blindness.
• It also predisposes to cardiovascular diseases. With an increasing incidence
worldwide, DM will be a leading cause of morbidity and mortality for the
foreseeable future.
• Types :DM type 1,DM type 2,Gestational DM.

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INTRODUCTION
The causes which are directly related to diabetes require differentiation:
-Hypoglycemic coma resulting from excessive doses of insulin or oral
hypoglycemic agents.
-Hyperglycemic coma associated with either severe insulin deficiency (diabetic
ketoacidosis) or mild to moderate insulin deficiency (hyperglycemic
hyperosmolar state).

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 HYPOGLYCEMIC COMA

• Spontaneous hypoglycemia in adults is of two principal types: fasting and

postprandial.
• Symptoms begin at plasma glucose levels in the range of 60 mg/dL and
impairment of brain function at approximately 50 mg/dL.
• Fasting hypoglycemia is often subacute or chronic and usually presents with
neuroglycopenia as its principal manifestation.
• Postprandial hypoglycemia is relatively acute and is often heralded by
symptoms of neurogenic autonomic discharge.

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HYPOGLYCEMIC COMA
 Signs and Symptoms
 Adrenergic hypoglycemia signs and symptoms include:
 Pallor ,Tremulousness, Nervous anxiety,
Irritability,Tachycardia,Diaphoresis,Weakness.
 Neuroglycopenic hypoglycemia signs and symptoms include:
 Diplopia, Lethargy, Inability to concentrate, Confusion, Behavior change,
Paresthesias, Hunger, Stupor, Seizure, Coma.

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HYPOGLYCEMIC COMA
 Management
• Oral treatment with glucose tablets or glucose-containing fluids.A reasonable
initial dose is 20 g of glucose.
• If the patient is unable or unwilling, Intravenous glucose (25 g) should be
given and followed by a glucose infusion guided by serial plasma glucose
measurements. Rules of 15 for children (15g recheck after 15 min if Glucose
<100 g/dl repeat the cycle).
• Glucagon 1.0 mg in adults,0.3 mg<6yrs,0.5 mg >6yrs in patients with T1DM.
• Patients should therefore be urged to eat as soon as is practical to replete
glycogen stores.

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DIABETIC KETOACIDOSIS(DKA)
 DKA results from relative or absolute insulin deficiency combined with
counterregulatory hormone excess (glucagon, catecholamines, cortisol, and
growth hormone).
 Both insulin deficiency and glucagon excess, in particular, are necessary for
DKA to develop.
 The decreased ratio of insulin to glucagon promotes gluconeogenesis,
glycogenolysis, and ketone body formation in the liver, as well as increases
in substrate delivery from fat and muscle (free fatty acids, amino acids) to the
liver.

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DKA
 Clinical findings
 Signs and symptoms
• Preceded by a day or more of polyuria and polydipsia associated with
marked fatigue, nausea and vomiting, and, finally, mental stupor→Coma.
• Dehydration in a stuporous patient with rapid deep breathing and a "fruity"
breath odor of acetone.
• Hypotension with tachycardia indicates profound fluid and electrolyte
depletion.
• Hypothermia.

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DKA

 Laboratory findings
• Hyperglycemia > 250 mg/dL.
• Acidosis with blood pH < 7.3
• Serum bicarbonate < 15 meq/L.
• Serum positive for ketones.
• Elevated blood urea nitrogen (BUN) and serum creatinine levels reflect
intravascular volume depletion.
• Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia.

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DKA

 Management

Admit to hospital; intensive-care setting may be necessary for frequent
monitoring or if pH < 7.00 or unconscious.

Assess:
• Serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate)
• Acid-base status—pH, HCO3-, PCO2, b-hydroxybutyrate
• Renal function (creatinine, urine output)

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DKA

Replace fluids:
• 2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour); subsequently,
0.45% saline at 150–300 mL/h;
• change to 5% Glucose and 0.45% Saline at 100–200 mL/h when plasma
glucose reaches 250 mg/dL (14 mmol/L).

Administer short-acting insulin:
• IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by
continuous IV infusion; increase 2- to 3-fold if no response by 2–4 h.
• If initial serum potassium is < 3.3 mmol/L (3.3 meq/L), do not administer
insulin until the potassium is corrected to > 3.3 mmol/L (3.3.meq/L).

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DKA
• Assess patient: What precipitated the episode (noncompliance, infection,
trauma, infarction, cocaine)? Initiate appropriate workup for precipitating
event (cultures, CXR, ECG).
• Measure capillary glucose every 1–2 h; measure electrolytes (especially K+,
bicarbonate, phosphate) and anion gap every 4 h for first 24 h.
• Monitor blood pressure, pulse, respirations, mental status, fluid intake and
output every 1–4 h.
• Replace K+: 10 meq/h when plasma K+ < 5.5 meq/L, ECG normal, urine flow
and normal creatinine documented; administer 40–80 meq/h when plasma
K+ < 3.5 meq/L or if bicarbonate is given.

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DKA
• Continue above until patient is stable, glucose goal is 150–250 mg/dL, and
acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg
per hour.
• Administer intermediate or long-acting insulin as soon as patient is eating.
Allow for overlap in insulin infusion and subcutaneous insulin injection

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HYPERGLYCEMIC HYPEROSMOLAR STATE(HHS)
• The prototypical patient with HHS is an elderly individual with type 2 DM.
• This second most common form of hyperglycemic coma is characterized by
• severe hyperglycemia in the absence of significant ketosis with a several
week history of polyuria, weight loss, and diminished oral intake that
culminates in mental confusion, lethargy, or coma.

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HHS
• Relative insulin deficiency and inadequate fluid intake are the underlying
causes of HHS.
• Insulin deficiency increases hepatic glucose production) and impairs glucose
utilization in skeletal muscle.
• Hyperglycemia induces an osmotic diuresis that leads to intravascular
volume depletion.
• Lower levels of counterregulatory hormones and free fatty acids have been
found in HHS than in DKA in some studies.

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HHS
 The physical examination
• Profound dehydration and hyperosmolality.
• hypotension, tachycardia, and altered mental status.
• HHS is often precipitated by a serious, concurrent illness such as myocardial
infarction or stroke. Sepsis, pneumonia, and other serious infections are
frequent precipitants and should be sough
• Notably absent are symptoms of nausea, vomiting, and abdominal pain and
the Kussmaul respirations characteristic of DKA.

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HHS
 Laboratory findings
• Hyperglycemia > 600 mg/dL.
• Serum osmolality > 310 mosm/kg.
• No acidosis; blood pH above 7.3.
• Serum bicarbonate > 15 meq/L.
• Normal anion gap (< 14 meq/L).
• In contrast to DKA, acidosis and ketonemia are absent or mild. A small anion
gap metabolic acidosis may be present secondary to increased lactic acid.
Moderate ketonuria, if present, is secondary to starvation.

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HHS
 Management
• Volume depletion and hyperglycemia are prominent features of both HHS
and DKA.
• Consequently, therapy of these disorders shares several elements
• Patient's fluid status, laboratory values, and insulin infusion.
• Underlying or precipitating problems should be treated.
• In HHS, fluid losses and dehydration are more pronounced than in DKA
• The patient with HHS is usually older, more likely to have mental status
changes.
• HHS has a substantially higher mortality than DKA.

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HHS
 Management

Fluids replacement
• 1–3 L of 0.9% normal saline over the first 2–3 h. As much as 4-6 L of fluid
may be required in the first 8-10 hours.
• If the serum sodium > 150 mmol/L (150 meq/L), 0.45% saline should be
used.
• Once blood glucose reaches 250 mg/dL, fluid replacement should include
D5W.

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HHS
 Management

Insulin infusion
• IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by
continuous IV infusion; increase 2- to 3-fold if no response by 2–4 h.
• As in DKA, glucose should be added to IV fluid when the plasma glucose
falls to 13.9 mmol/L (250 mg/dL), and the insulin infusion rate should be
decreased to 0.05–0.1 units/kg per hour.
• Avoid cerebral edema ,if present give IV mannitol dose 0.2 to 1 g/kg

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SUMMARY
PHYSICAL FINDINGS HYPOGLYCEMIC COMA HYPERGLYCEMIC COMA
• pulse rate ↑↑ ↑↑
• pulse volume full weak
• temperature ↓↓↓ ↓↓↓
• respiration shallow or normal rapid and deep
• blood pressure normal, ↑↑ ↓↓↓
• skin clammy, sweating dry
• Tongue moist dry
• tissue turgor normal eyeball tension normal reduced
• breath no acetone acetone may be present
• reflex brisk reflexes diminished reflexes

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SUMMARY
LABORATORY TEST HYPOGLYCEMIC COMA HYPERGLYCEMIC COMA

• Urine glucose -ve to +ve +ve

• Plasma glucose -ve to +ve > 200mg/dl
• Plasma acetone -ve present
• Plasma bicarbonate normal < 20mg/litre
• Plasma CO2 normal diminished
• Blood pH normal < 7.35

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 Thank You

14TH November–World Diabetes Day

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