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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