Acute Complications of

Diabetes-Reshma Ann Mathew

DIABETES

It is a GROUP of metabolic disease characterised by chronic hyperglycemia with DISTURBANCE in the carbohydrate, fat & protein metabolism resulting from DEFECTS in insulin secretion, insulin action or both .

Pancreas beta cells

Insulin actions

Glucose entry and utilization (oxidation, storage)

Glucose entry and oxidation

TG synthesis

Normal glucose and fat metabolism

Pancreas beta cells

Insulin actions

Glucose entry and utilization (oxidation, storage)

Glucose entry and oxidation

TG synthesis

Metabolic consequences of insulin deficiency/resistance

Clinical Features of DM due to insulin lack

Polyphagia(decr. leptin?)

Starvation in the midst of plenty

Hyperosmolar hyperglycemic syndrome (HHS)

Lactic acidosis

Lactic acidosis

Muscle protein breakdown

Acetoacetate,0H-butyrate, acetone

• Insulin level increases when?a) Glucose administered by mouth (food intake)b) Glucose given by IV (glucose infusion)c) No difference

CLASSIFICATION1) Type 12) Type 23) Other specific types4) Gestational diabetes

DIABETIC KETOACIDOSIS

• It is a MEDICAL emergency• PRINCIPALLY seen in type 1 diabetes• Mortality-

• CHILDREN & ADOLESCENTS- cerebral edema• ADULTS- hypokalemia, acute respiratory distress syndrome

& co-morbid conditions

PATHOPHYSIOLOGY

InsulinCounterregulatory hormones

Glucagon, Epinephrine, Cortisol, Growth hormone

NORMAL

EXCESS counterregulatory hormones

Insulin DEFICIENCY

DKA

Insulin DeficiencyGlucose uptake

ProteolysisLipolysis

Amino Acids

Glycerol Free Fatty Acids

GluconeogenesisGlycogenolysisHyperglycemia

Hepatic Ketogenesis

Metabolic Acidosis

Osmotic diuresis

Dehydration & electrolyte loss

Excess counterregulatory hormones

Forces H+ ions into cells & displaces K+

Ketosis

• The cardinal biochemical features are-1) Hyperketonemia (> 3mmol/L) & Ketonuria (> 2+ on standard

urine sticks)2) Hyperglycaemia (blood glucose > 200mg/dL)3) Metabolic acidosis (venous bicarbonate <15mmol/L and/or

venous pH<7.3)

Insulin Deficiency

Glucose uptake Proteolysis Lipolysis

Amino AcidsGlycerol Free Fatty Acids

GluconeogenesisGlycogenolysis

Hyperglycemia Ketogenesis

Acidosis

Osmotic diuresis

Polyuria, Polydipsia

Fruity breath (acetone smell)Kussmaul breathing (acidotic)Mental status changes

Dehydration (Dry tongue, Tachycardia, Hypotension)Abdominal pain

Electrolyte imbalance

Clinical manifestations

MANAGEMENTInvestigations-

oVENOUS BLOOD- for urea, electrolytes, glucose & bicarbonatesoARTERIAL BLOOD GAS- to assess severity of acidosisoURINE- for ketonesoECGoINFECTION SCREEN

Treatment-1) SHORT ACTING SOLUBLE insulin2) Fluid replacement- 0.9% saline (NaCl)3) Potassium replacement4) Sodium bicarbonate- in SEVERELY ACIDOTIC patients5) Antibiotics- if INFECTION is present

COMPLICATIONS1) Cerebral edema- due to RAPID REDUCTION of blood glucose,

USE of hypotonic fluids and/or bicarbonates2) ARDS (Acute Respiratory Distress Syndrome)3) Thromboembolism4) DIC(Disseminated Intravascular Coagulation)5) Acute Circulatory Failure

Hyperglycaemic Hyperosmolar State

HSS occurs due to-• Relative INSULIN DEFICIENCY• Inadequate FLUID INTAKE

PATHOPHYSIOLOGY

Insulin deficiency

SEVERE HYPERGLYCEMIA

GLUCOSURIA

WEIGHT LOSS

OSMOTICDIURESIS

POLYURIAPOLYDIPSIA

LIPOLYSISWithout

KETOSIS

SEVEREOSMOTIC

DEHYDRATION

• It is characterised by1) SEVERE hyperglycaemia (>600mg/dL)2) Hyperosmolality (serum osmolality >320 mOsm/kg)3) Dehydration (in the ABSENCE of significant hyperketonemia or

acidosis)

CLINICAL MANIFESTATIONS• Polyuria, weight loss, and diminished oral intake• Profound dehydration• Hypotension, tachycardia and altered mental status• Mental confusion, lethargy or coma

MANAGEMENT• Normalise osmolality- 0.45% saline• Replace fluid and electrolyte losses• Normalise blood glucose

HYPOGLYCEMIA

• Hypoglycemia (<63mg/dL) in DIABETES occurs due to insulin overdose or hyperinsulinemia

• Whipple’s triad-a) Symptoms consistent with HYPOGLYCEMIAb) Low plasma glucose conc. (measured with a precise method)c) Relief of symptoms after plasma glucose level is RAISED

Causes of Hypoglycemia in patients taking insulin

Missed, delayed or inadequate mealUnexpected or unusual exerciseAlcoholErrors in oral anti-diabetics or insulin

dose/schedule/administrationPoorly designed insulin regimenLipoatrophy at injection sitesFactitous (deliberately induced)Breasting feeding by DIABETIC mother

NORMAL

When blood glucose level FALLS

Endogenous insulin release is SUPRESSED

Release of glucagon is

INCREASED

Autonomic nervous system is ACTIVATED

Release of catecholamine; stress hormones are

INCREASED in blood

REDUCTION of whole blood glucose uptake & INCREASES

hepatic glucose production

Thus, maintaining glucose supply to brain

TYPE 1 DIABETES

CANNOT regulate insulin once it is injected subcutaneously

Hypoglycemia

Symptoms-1)Autonomic2)Neuroglycopenic3)Non-specific

MANAGEMENTMILD (self treated)• Oral fast acting carbohydrate (10-15g) is taken as glucose drink

or tablets or confectionery• Followed with a snack containing complex carbohydrate

SEVERE

• If patient is SEMI-CONSCIOUS OR UNCONSCIOUS-oIV 75mL 20% dextrose (0.2g/kg in children) OR IM glucagon

(0.5mg in children)• If patient is CONSCIOUS and able to SWALLOW-oGive oral refined glucose as drink or sweets (25mg)

Dawn phenomenon & Somogyi effect• DAWN PHENOMENON occurs when endogenous insulin

secretion decreases• SOMOGYI EFFECT is seen in cases of excessive amounts of

exogenous insulin

SOMOGYI EFFECT

TOO MUCH INSULIN

HYPOGLYCEMIA

GLUCAGON IS RELEASED

LIPOLYSISGLUCONEOGENESISGLYCOGENOLYSIS

REBOUNDHYPERGLYCEMIA

+KETOSIS

DAWN PHENOMENON Body’s response to hormones released in early morning hours

Counter-regulatory hormones are released

Glucose level increases

In DM, there is decrease in insulin levelsSo HIGH GLUCOSE levels in morning

DKA vs. HHSHHS DKA

More in elderly More in children Age

More in type II More in type I DM type

> 600 > 250 Glucose

+ or - +++++ Ketonuria/emia

>7.3 <7.3 pH

>15 <15 HCO3

Hyperosmolarity Variable S osmolarity

Sensitive to small dose Variable Sensitivity to insulin

DKA vs. HYPOGLYCEMIAHypoglycemia DKA

Insulin overdose or hyperinsulinemia

Insulin deficiency or increased counter-reg hormones

Etiology

Acute Gradual Onset

-S of Brain glucopenia- S of sympathetic overactivity

S of hyperglycemiaS of dehydration S of acidosis

Symptoms and signs

hypoglycemia hyperglycemia RBS

No Yes Ketonuria

No Yes Ketonemia

Rapidly recover if early No effect IV glucose

THANKYOU