final acute complications of diabetes mellitus

ACUTE COMPLICATIONS OF

DIABETES MELLITUS

Dr.Sandeep yadav

ACUTE COMPLICATIONS OF

DIABETES MELLITUS

1)Diabetic ketoacidisis• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment

2)Non ketotic hyperglycemic hyper osmolar coma• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment

3)Lactoacidosis• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment

4)Hypoglycemic AND Hypoglycaemic coma• Precipitating factors• Signs, symptoms, physical examination, laboratory findings• Treatment

Hyperglycemia

Ketosis

Acidosis

*

Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical

Studies in Medical Biochemistry. New York, NY: Oxford University Press; 1987:105.

Definition of Diabetic Ketoacidosis*

4

Precipitating factors of DKA

• Newly Diagnosed Diabetes (Presenting Manifestation

• Inadequate Administration Of Exogenous Insulin;

ABSOLUTE INSULIN

DEFICIENCY

• Inadequate Administration Of Exogenous Insulin

• An Intercurrent Infection (Pneumonia, Cholecyctitis);

• A Vascular Disorder (Myocardial Infarction, Stroke);

• An Endocrine Disorder(hyperthyroidism, Pheochromocytoma);

• Trauma;• Pregnancy;• Surgery

RELATIVE INSULIN

DEFICIENCY

7

Electrolyte LossesRenal Failure

Shock CV Collapse

Insulin Deficiency8

Hyperglycemia

Hyper-osmolality

Δ MS

Glycosuria

Dehydration

Lipolysis

FFAs

Acidosis

Ketones

CV Collapse

Insulin Deficiency9

Electrolyte LossesRenal Failure

Shock CV Collapse

Insulin Deficiency10

Hyperglycemia

Hyper-osmolality

Δ MS

Lipolysis

FFAs

Acidosis

Ketones

CV Collapse

Glycosuria

Dehydration

Diabetic Ketoacidosis: PathophysiologyUnchecked gluconeogenesis Hyperglycemia

Osmotic diuresis Dehydration

Unchecked ketogenesis Ketosis

Dissociation of ketone bodies into

hydrogen ion and anions

Anion-gap metabolic

acidosis

11

• Often a precipitating event is identified (infection, lack of insulin

administration)

12

Clinical Presentation of

Diabetic KetoacidosisHistory Physical Exam

• Thirst

• Polyuria

• Abdominal pain

• Nausea and/or vomiting

• Profound weakness

• Kussmaul respirations

• Fruity breath

• Relative hypothermia

• Tachycardia

• Supine hypotension, orthostatic drop of blood pressure

• Dry mucous membranes

• Poor skin turgor

13

Initial Laboratory Evaluation of DKA

• Comprehensive metabolic profile

• Serum osmolality

• Serum and urine ketones

• Arterial blood gases

• CBC

• Urinalysis

• ECG

14

Treatment

REFERENCES:

1) American Diabetic Association

2) British Medical Journal

3) E-medscape

4) Harisson Principle Of Internal Medicine 18th

Edition

5) British Society Of Paediatric Endocrinology

And Diabetes

The goals of therapy include:

1.Rehydration

1.Reduction of hyperglycemia

2.Correction of electrolyte imbalance

3. Correction of acid-base imbalance

4.Investigation of precipitating factors, treatment of complications.

FLUIDSFLUID RESUSCITATION IS A CRITICAL PART

OF TREATING PATIENTS WITH DKA. Intravenous solutions replace extravascular and

intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels

of circulating counterregulatory hormones. Fluid it self leads to correction of acidosis to some

extentInsulin is needed to help switch from a catabolic

state to an anabolic state, with uptake of glucose in tissues and the reduction of gluconeogenesis as well as free fatty acid and ketone production

0.9 % NaCl(15-20 ml/kg/hr)

Administer 1-3 L during the first hour.

Administer 1 L during the second hour

Administer 1 L during the following 2 hours

Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings

In general, 0.45% NaCl infused at 4–14 ml · kg−1 ·

h−1 is appropriate if the corrected serum sodium is

normal or elevated

INSULIN RECOMENDATIONS

In adult patients, (IfK+ <3.3 mEq/l) , an IV bolus of regular insulin at 0.15 u/kg body wt

continuous infusion of regular insulin at a dose of 0.1 unit · kg−1 · h−1 (5–7 units/h in adults), should be administered

If plasma glucose does not fall by 50 mg/dl from the initial value in the 1st hour, check hydration status; if acceptable, the insulin infusion may be doubled every hour until a steady glucose decline between 50 and 75 mg/h is achieved.

When the plasma glucose reaches 250 mg/dl in DKA or 300 mg/dl in HHS, it may be possible to decrease the insulin infusion rate to 0.05–0.1 unit · kg−1 · h−1 (3–6 units/h), and dextrose (5–10%) may be added to the intravenous fluids.

Initiate subcutaneous insulin at least 2 h before interruption of insulin infusion

Potassium Repletion in DKA

• K+ >5.2 mEq/L▫ Do not give K+ initially, but check serum K+ with

basic metabolic profile every 2 h▫ Establish urine output ~50 mL/hr

• K+ <3.3 mEq/L▫ Hold insulin and give K+ 20-30 mEq/hr until

K+ >3.3 mEq/L

• K+ = 3.3-5.2 mEq/L▫ Give 20-30 mEq K+ in each L of IV fluid to

maintain serum K+ 4-5 mEq/L

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Phosphorus Repletion in DKA

• A sharp drop of serum phosphorus can also occur during insulin treatment

• Treatment is usually not required

▫ Caregiver can give some K+ as K- phos

23

CORRECTION OF ACID BASE BALANCE

Its role is controversial

Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis

It is recommended for patients in shock and/or if pH is <6.9

Treatment of Concurrent Infection

• In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Starting empirical antibiotics on suspicion of infection until culture results are available may be advisable.

Criteria for resolution of DKA

glucose <200 mg/dl,

serum bicarbonate ≥18 mEq/l, and

venous pH of >7.3.

Once DKA is resolved, if the patient is NPO, continue intravenous insulin and fluid replacement and supplement with subcutaneous regular insulin as needed every 4 h.

Nonketonic hyperglycemic-hyperosmolar

coma (NKHHC or HNC).

HNC is a syndrome characterized by impaired consciousness, sometimes accompanied by seizures, extreme dehydration, , and extreme hyperglycemia that is not accompanied by ketoacidosis.

HHS

CEREBROVASCULAR

ACCIDENTS,PANCREATITIS,BURN

INFECTIONS(PNUEMONI

A,UTI)

DRUGS (STEROIDS,THIAZIDE

S)

Physical examination

1. Severe dehydration is invariably present.

2. Various neurologic deficits (such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia) are commonly present. Altered states of consciousness from lethargy to coma are observed.

3. Findings associated with coexisting medical problems (e.g., renal disease, cardiovascular disease) may be evident.

Laboratory findings1. Extreme hyperglycemia (blood glucose levels from

30 mmoll/l and over are common.

2. A markedly elevated serum osmolality is present, usually in excess of 350 mOsm/l. (Normal = 290 mOsm)

3. Serum ketones are usually not detectable, and patients are not acidic.

4. Serum sodium may be high (if severe degree of dehydration is present), normal, or high

5. Serum potassium levels may be high (secondary to the effects of hyperosmolality) Low or normal

DKA and HHS Are Life-Threatening

EmergenciesDiabetic Ketoacidosis (DKA)

Hyperglycemic Hyperosmolar State (HHS)

Plasma glucose >250 mg/dL Plasma glucose >600 mg/dL

Arterial pH <7.3 Arterial pH >7.3

Bicarbonate <15 mEq/L Bicarbonate >15 mEq/L

Moderate ketonuria or ketonemia Minimal ketonuria and ketonemia

Anion gap >12 mEq/L Serum osmolality >320 mosm/L

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Treatment

This condition is a medical emergency and the patient should be placed in an intensive care unit.

Many of the management techniques recommended for a patient with DKA are applicable here as well.

The goals of therapy include:

• rehydration;

• reduction of hyperglycemia;

• electrolytes replacement;

• investigation of precipitating factors, treatment of complications.

Lactic acidosis (LA).

DM is one of the major causes of LA, a serious condition characterized by excessive accumulation of lactic acid and metabolic acidosis.

The hallmark of LA is the presence of tissue hypoxemia, which leads to enhanced anaerobic glycolysis and to increased lactic acid formation.

The normal blood lactic acid concentration is 1 mmol/l, and the pyruvic to lactic ratio is 10:1. An increase in lactic acid without concomitant rise in pyruvate leads to LA of clinical importance.

Predisposing factors

1. Heart and pulmonary failure (which leads to hypoxia)

2. Alcohol intoxication.

3. Ketoacidosis (it is important to have a very high index of suspection with respect to presence of LA).

Physical examination

1. Acrocyanosis is common.2. Tachycardia frequently is present, blood

pressure is decreased.3. Poor skin tugor and dry skin may be

prominent.4. Hypothermia is common in LA.5. Hyperpnea or Kussmaul respiration are

present and related to degree of acidosis.6. Findings associated with coexisting medical

problems (e.g., renal disease, cardiovascular disease) may be evident.

Laboratory findings

1. Blood glucose level is not high

2. Glucosurea is absent.

3. Blood lactic acid is high.

Treatment of LA

LA is treated by correcting the underlying cause.1. Oxygentherapy2. Metyleneblue (50 – 100 ml of 1 % solution i/v

droply)3. In severe cases, bicarbonate therapy should be

used (intravenously-infused 2,5 % sodium bicarbonates 1 to 2 l/day).

4. LA can be treated with low dose insulin regimens with 5 % glucose solution infusion.

5. Symptomatic therapy:- Hydrocortisone (250 mg i/v)- Unitiol (5% solution 10 ml i/v (1- 2 ml/10 kg)- α-lipoid acid (berlition, espa-lipon)

Comparison of DCA, HNC and LA.

Hypoglycemia

It is a syndrome characterized by symptoms of sympathetic nervous system stimulation or central nervous system dysfunction that are provoked by an abnormally low plasma glucose level.

Hypoglycemia represents insulin excess and it can occur at any time.

Precipitating factors

• irregular ingestion of food;

• extreme activity;

• alcohol ingestion;

• drug interaction;

• liver or renal disease;

• hypopituitarism and adrenal insufficiency.

Physical examination

1. The skin is cold, moist.

2. Hyperreflexia can be elicited.

3. Hypoglycemic coma is commonly associated with abnormally low body temperature

4. Patient may be unconsciousness.

Treatment

• The most effective treatment of an insulin reaction is the immediateingestion of a concentrated carbohydrate source, such as sugar,honey, candy, or orange juice.

• Alternative methods for increasing blood glucose may be requiredwhen the person having the reaction is unconscious or unable toswallow:▫ Glucagon may be given intramuscularly or subcutaneously.▫ In situations of severe or life-threatening hypoglycemia, it may be

necessary to administer glucose intravenously.

PREVENTION IS BEST CURE