acute diabetic complication dr. mohamed ibrahim (1) (1)

Dr. Mohamed Ibrahim Youssef

Family Medicine Specialist

Albassam Diabetic Center

Diabetic ketoacidosis (DKA).

Hyperosmolar hyperglycemic State.

Hypoglycemia.

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)are two of the most serious acute complications of diabetes.

DKA=hyperglycemia ,ketosis , acidosis.

HHS= hyperosmolarity , hyperglycemia ,altered mental status.

DKA = 3 letters= triad of D K A

Diabetic glucose >250 mg/dL

Ketoketones – both in urine and in serumacetoacetate, acetone, betahydroxybutyratefruity smell. If the Ketone level is below 0.6 mmol/L is normal.The person with a reading above 1.5 mmol/L indicate a greater risk for developing Ketoacidosis (DKA).

AcidosisIncreased anion gap AG=[(Na)-(Hco3+CL)],metabolic acidosis; HCO3-

<15, pH<7.30

The normal blood pH is tightly regulated between 7.35 and 7.45.

Traditional teaching # reality

Traditional

DKA seen in type1,<65 year old.

HHS seen in type2,>65 year old.

Reality

Most patients with DKA or HHS have type 2 DM , and

many patients with DKA are >65 years old

Hyperglycemia ↑Insulin

↑Glucose uptake↓Glucose production

↓Gluconeogenesis ↓Glycogenolysis

Normoglycemia

Hyperglycemia ↑Insulin

↓Glucose uptake↑Glucose production

↑ Gluconeogenesis ↑ Glycogenolysis

Hyperglycemia

Infection i.e. (Pneumonia,

sepsis,UTI)

Inadequate insulin

Inadequate water intake

Infarction (myocardial)

Intoxication(cocaine)Recurrent DKA

Ischaemic(Stroke)

injury

Insult (Emotional)

Infant(Pregnancy)

New onset type 1

(20 to 25 %)

Drugs.

I

DKA

HHS

DKA evolves rapidly, over 24-hour period.

Hhs develop more insidiously (days).

Polyuria, polydipsia, and weight loss.

Fatigue ,dyspnea , vomiting, preceding febrile illness ,and

polyphagia .

Dehydration( tachycardia, poor skin turgor, dry mucous

membranes, and orthostatic hypotension) .

Neurologic symptoms(hemiparesis, hemianopsia or seizures)

are most common in hhs.

Hyperventilation and abdominal pain with dka.

• Abdominal pain

It is more common in children, unusual in HHS

It is multifactorial

Metabolic acidosis. Not hyperglycamiea.?pancreatitis

Delayed gastric emptying.

Ileus from electrolyte disturbances

It sometimes mimicks acute abdomen.

Insulin Deficiency

Glucose uptakeProteolysis

Lipolysis

Amino Acids

Glycerol Free Fatty Acids

Gluconeogenesis

GlycogenolysisHyperglycemia

Ketogenesis

Acidosis

Osmotic diuresis

PolyuriaPolydipsia

DehydrationDry tongue ,Tachycardia ,Hypotension

Fruity breath (acetone smel) nail polish removerKussmaul breathing (acidotic)Mental status changes

Electrolyte imbalance

Clinical manifestations

DD of acidotic breathing◦ Renal failure.

◦ Amonia increase in HCF.

◦ Hysterical .

DD of diabetic coma◦ Lactic acidosis

◦ Hyperosmolar non-ketotic coma.

◦ Hypoglycemia .

DD of coma in general.

DD of acute abdomen.

HHSDKA

More in elderlyMore in childrenAge

More in type IIMore in type IDM type

> 600> 250Glucose

+ or -+++++Ketonuria/emia

>7.3<7.3pH

>15<15HCO3

HyperosmolarityVariable S osmolarity

Sensitive to small doseVariable Sensitivity to insulin

HypoglycemiaDKA

Insulin overdose or hyperinsulinemia

Insulin deficiency or increased counter-reghormones

Etiology

Acute Gradual Onset

-S of Brain glucopenia- S of sympathetic overactivity

S of hyperglycemiaS of dehydration S of acidosis

Symptoms and signs

hypoglycemiahyperglycemia RBS

No Yes Ketonuria

No YesKetonemia

Rapidly recover if earlyNo effectIV glucose

Golden ruleAny diabetic patient with DKA versus hypoglycemia, give

glucose even before glucose measuring

Diagnosis

Triad for diagnosis

Hyperglycemia > 300 mg/dl

Ketonemia and ketonuria(Direct assay of beta-

hydroxybutyrate levels is preferred)

Blood gas metabolic acidosis

pH < 7.3

High anion gap =(Na ) – (Cl + HCO3) > 10 may reach 20

and

Bicarbonate <15 mEq/L

Direct measure

oxidation

May be absent in mild cases

For diagnosis

Other findings◦ Electrolyte serum level

Hyperkalemia (rarely Hypokalemia),

Hyponatremia (rarely Hypernatremia )

◦ Investigation for the cause such as

Urine Analysis, AMI panel and ECG, Chest x-ray

◦ Hyperosmolarity

Normal = 285-295 (mOsmol/kg)

For monitoring

RBS :every 1 hour till RBS reaches 200 mg/dl or

less, then every 6 hours

Venous ph (for DKA) every two to four hours.

Direct measurement of beta-

hydroxybutyrate(not urine ketones)

Electrolytes serum level every 4 hours till

correction

Treatment of predisposing factors.

Initial hospital management

◦ Care of comatosed patients(Airway, breathing, and circulation (ABC) status

◦ I.V fluids◦Electrolytes replacement.◦ Insulin .◦ Treatment of complications if happen.

Once resolved

◦ Convert to home insulin regimen.

◦ Prevent recurrence.

Fluid deficit 3-6 liters for DKA and 8-10liters in HHS.

Over 24 hours.

Patients with hypovolemic shock. Isotonic saline as

quickly as possible.

Patients without shock (and without heart failure),

isotonic saline 15 to 20 ml/kg for the first 2 hours.

Then according to state of hydration, serum

electrolyte levels, and the urine output.

Measure “corrected” sodium .

Add dextrose to the saline solution when the

serum glucose reaches

200 mg/dl (11.1 mmol/L) in DKA or 250 to

300 mg/dl (13.9 to 16.7 mmol/L) in HHS

◦ If Hyperkalemia (> 5.3 meq/L)

initially present.

No treatment as it resolves quickly with insulin.

◦ If normal level (3.3-5.3 meq/L)

Add (20-30) mEq for each Liter of infused fluid.

◦ If Hypokalemia (<3.3meq/L)

Add 40 mEq for each Liter of infused fluid.

Not recommend for routine use .

considered if severe hypophosphatemiaoccurs..what symptoms .

When needed, potassiumor sodium phosphate 20 to 30 meq can be added to 1 litter of IV fluids.

Bicarbonate given if the arterial

PH is less than 6.90.

We give 100 meq of sodium

bicarbonate in 400 ml sterile

water with 20 meq

of potassium chloride, if the

serum potassium is less than

5.3 meq/L, administered over

two hours.

• IV bolus of 0.1 units/kg regular insulin.

• Infusion insulin at 0.1 units/kg/hr

• (Check BG every 1hour.

• ( goal of reduction is 50-80 mg/dl/hr)

When reaches

◦ 200 mg/dL in DKA or 250 to 300 mg/dL in HHS, the

IV saline solution is switched to dextrose in

saline, and decrease the insulin infusion rate to 0.02

to 0.05 U/kg per hour.

DKADKA

HHSHHS

Infection

◦ Precipitates DKA

◦ Leukocytosis can be

secondary to acidosis

Shock

◦ If not improving with fluids

r/o MI

Vascular thrombosis

Pulmonary Edema

◦ Result of aggressive fluid

resuscitation

Cerebral Edema

◦ First 24 hours due to aggressive

correction of hyperglycemia or

administration of hypotonic

solution

◦ c/p: Mental status changes

◦ Tx: Mannitol

◦ May require intubation with

hyperventilation

Never omit insulin.

Prevent dehydration and hypoglycemia.

Monitor blood sugars frequently.

Monitor for ketosis.

Provide supplemental fast acting insulin.

Treat underlying triggers.

Maintain contact with medical team.

Plasma glucose is usually high but not always.

◦ DKA can be present with RBS < 300 due to

Impaired gluconeogenesis

Liver disease

Acute alcohol ingestion

Prolonged fasting.

Pregnancy.

Ketone (acetoacetic acid by nitroprusside tablets (Acetest)or

reagent sticks (Ketostix) in urine may be –ve in DKA, but

always +ve in blood(betahydroxybuteric acid which is the

predominant ketone)

High WBC may be present without infection.>>>Bandaemia

High creatinine may be present without true renal function(it

may cross react with ketone bodies).

Blood urea may be elevated with prerenal azotemia

secondary to dehydration.

Serum amylase is often raised even in the absence of

pancreatitis.

Creatine kinase and troponin levels mildly increase in the

absence of myocardial damage

Definition:

◦ In diabetic patients if low plasma glucose

concentration≤70 mg/dl. (With or without

symptoms)

Clinical classification:◦ Severe hypoglycemia.

◦ Documented symptomatic hypoglycemia .

◦ Asymptomatic hypoglycemia.

◦ Probable symptomatic hypoglycemia

◦ Pseudohypoglycemia

Symptoms.

Risk factor assessment:◦ Ask about hypoglycemia at every visit.

◦ Review the self-monitoring of blood glucose (SMBG)

Prevention:◦ consider more modest goals for A1C values.

◦ Education.

Treatment

For asymptomatic or symptomatic hypoglycemia ,ingest

carbohydrates. 15 to 20 grams of oral glucose is typically

sufficient. Glucose may be ingested in the form of tablets,

juice, milk,

glucagon(0.5 to 1.0) mg given as a subcutaneous or

intramuscular injection. If difficult IV access .(or at home)

EDUCATION .

IV dextrose (25 g of 50 percent glucose [dextrose]) can be

administered to treat hypoglycemia in patients with

impaired consciousness and established IV access

(typically in hospital).

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