DIABETIC

EMERGENCY
BY DR CHANDRIMA PATTADAR
 INTRODUCTION
• Diabetic ketoacidosis and hyperglycemic hyperosmolar state are acute
metabolic complications of diabetes mellitus that can occur in patients with
both type 1 and 2 diabetes mellitus.
Diabetic ketoacidosis
 ABSOLUTE OR RELATIVE INSULIN INCREASES COUNTERREGULATORY HORMONES
DEFICIENCY LIKE GLUCAGON, CATECHOLAMINES

CANT INHIBIT HORMONE INCREASED INCREASED

DECREASED GLUCOSE
SENSITIVE LIPASE IN GLUCONEOGENESIS GLYCOGENOLYSIS
UTILIZATION
ADIPOSE TISSUE

TAG FFA HYPERGLYCEMIA

EXCEEDS RENAL THRESHOLD OF GLUCOSE ABSORPTION
INCREASED PRODUCTION OF GLYCOSURIA
ACETYL COA THROUGH B Osmotic diuresis
OXIDATION LOSS OF WATER
AND ELECTROLYTES
KETOGENESIS IN LIVER
KETONE YIELDS ENERGY – 4lcal/g
DEHYDRATION GLUCOSE – 3.7kcal/g
METABOLIC ACIDOSIS
IMPAIRED RENAL
FUNCTION

USED BY HEART CNS

• Normal concentration ketones in blood is 0.1 mmol/L

• Acetoacetate and betahydroxybutyrate are strig acids, and promote a decrease

in plasma pH when their plasma conc reach 3mmol/L

• In diabetic ketoacidosis, Acetoacetate : betahydroxybutyrate = 1:3

• Ketostix detects acetoacetate : minimum conc required of 3 mmol/L , not able to

detect : betahydroxybutyrate
• So it is insensitive method to detect ketoacidosis
 EPIDEMIOLOGY
• DKA accounts for 14% of all hospital admissions of patients with
diabetes .
• 16% of all diabetic related fatalities
• It is seen slightly higher in females ( cause is not clear)
• Type 1 DM > Type 2 DM
 DIABETIC KETOACIDOSIS
• Blood glucose > 250mg /dl,
• plasma pH <7.3,
• plasma HCO3 <18 mEq/L
• Evidence of ketones in blood or urine
• Elevated anion gap
Exception :
1.in 20% cases, blood glucose is mildly elevated(<250mg/dl, patients who have
poor oral intake, received insulin prior to arrival in the emergency department,
pregnant woman , those who use SGLT2 inhibitors).
2.anion gap can be normal
Precipitating events :
• Inadequate insulin administration
• Infection (pneumonia/UTI/ gastroenteritis/sepsis)
• Infarction (cerebral, coronary, mesenteric, peripheral)
• Trauma
• Drugs (cocaine)
• Pregnancy
 Symptoms :

• Nausea/vomiting (due to ketoacids , particularly with beta hydroxybutyrate)

• Thirst/polyuria
• polydipsia
• Abdominal pain
• Shortness of breath
• As hyperglycemia worsens, the combined effect of serum hyperosmolarity,
dehydration , acidosis result in increased osmolarity in brain cells, then
neurologic symptoms appear and may progress to lethargy, focal deficit,
seizure, coma.
 Physical Findings:

• Tachycardia
• Dehydration(dry skin, dry mucous membrane, decreased skin turgor)
• Hypotension
• Tachypnea/Kussmaul respirations/ respiratory distress
• Fruity odor ( due to acetone)
• Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen)
• LethargY/cerebral edema/possibly coma
 INVESTIGATION
• RBS stat
• ABG stat
• URINE ketostix stat ( measure acetoacetic acid , not betahydroybutyrate)
• CBC
• LFT
• KFT
• Serum ketone( beta hydroxybutyrate)
• BLOOD C/S
• URINE R/E,M/E , C/S
• Calculate plasma osmolality
• ECG
• Chest Xray
 Treatment and Monitoring
• Maintain airway, breathing, circulation.
• Obtain large bore IV canula
• If the patient is vomiting or has altered mental status, a nasogastric tube should be inserted to prevent aspiration of
gastric contents.
• Monitor – serum glucose hourly until the patient is stable
• Monitor – electrolytes , pH , HCO3 every 2-4 hours until the patient is stable
• Determine and treat underlying cause of DKA
 FLUID THERAPY
• Volume deficit in DKA = 50-100ml/kg ( for 60 kg person, deficit is near about 3-5 ltr)
 2–3 L of 0.9% saline over first 1–3 h (10–20 mL/kg per hour);
 After intravascular volume is restored, start 0.45% saline at 250–500 mL/h ( if the corrected Na
level is normal or elevated , otherwise continue with isotonic saline);
 change to 5% glucose and 0.45% saline at 150–250 mL/h when plasma glucose reaches 200-250
mg/dL (13.9 mmol/L) to maintain the plasma glucose in the 8.3–11.1 mmol/L (150–200 mg/dL)
range.
• Active euglycemia is not recommended because of the risk of hypoglycemia
• The change to 0.45% saline helps to reduce the trend toward hyperchloremia later in the course of
DKA. Alternatively, initial use of lactated Ringer’s IV solution may reduce the hyperchloremia that
commonly occurs with normal saline.
 POTASSIUM CORRECTION
 Potassium stores are depleted in DKA (estimated deficit 3–5 mmol/kg [3–5 meq/kg])

Reason- insulin-mediated potassium transport into cells, resolution of the acidosis (which also promotes potassium entry
into cells), and urinary loss of potassium salts of organic acids

 Potassium correction ( Before starting Insulin )

 If Serum K level is 3.3 mEq/l, replace 20–40 meq of potassium in each liter of IV fluid is reasonable until K level is
above 3.3meq/L
 If initial Serum K level is 3.3 – 5.3 mEq/L replace 20–30 meq of potassium in each liter of IV fluid is reasonable and
maintaim K level 4 to 5 meq/L
 If K level is > 5.3 mEq/L , start insulin therapy.

To reduce the amount of chloride administered, potassium phosphate or acetate can be substituted for the chloride salt. The
goal is to maintain the serum potassium at >3.5 mmol/L (3.5 meq/L )
 INSULIN
• Bolus of IV (0.1 units/kg) short-acting regular insulin is usually administered immediately

• IV administration is usually preferred (0.1 units/kg of regular insulin per hour) because it ensures rapid
distribution and allows adjustment of the infusion rate as the patient responds to therapy

• IV regular insulin should be continued until the acidosis resolves and the patient is metabolically stable.

• As the acidosis and insulin resistance associated with DKA resolve, the insulin infusion rate can be decreased (to
0.02–0.1 units/kg per hour).

• Long-acting insulin, in combination with SC short-acting insulin, should be administered as soon as the patient
resumes eating, because this facilitates transition to an outpatient insulin regimen and reduces length of hospital
stay.
• Allow for a 2–4 hour overlap in insulin infusion, even relatively brief periods of inadequate insulin administration
in this transition phase may result in DKA relapse.

Hyperglycemia usually improves at a rate of 4.2–5.6 mmol/L (50–100 mg/dL) per hour as a result of insulin-mediated
glucose disposal, reduced hepatic glucose release, and rehydration
• Ketoacidosis begins to resolve as insulin reduces lipolysis, increases peripheral ketone body use, suppresses
hepatic ketone body formation, and promotes bicarbonate regeneration. However, the acidosis and ketosis
resolve more slowly than hyperglycemia.

• As ketoacidosis improves, β-hydroxybutyrate is converted to acetoacetate. Ketone body levels may appear to
increase if measured by laboratory assays that use the nitroprusside reaction, which only detects acetoacetate
and acetone. The improvement in acidosis and anion gap, a result of bicarbonate regeneration and
decline in ketone bodies, is reflected by a rise in the serum bicarbonate level and the arterial pH.

• Depending on the rise of serum chloride, the anion gap (but not bicarbonate) will normalize. A hyperchloremic
acidosis (serum bicarbonate of 15–18 mmol/L [15–18 meq/L]) often follows successful treatment and
gradually resolves as the kidneys regenerate bicarbonate and excrete chloride.
 HCO3 REPLACEEMENT

• Despite a bicarbonate deficit, bicarbonate replacement is not usually necessary.

In fact, theoretical arguments suggest that bicarbonate administration and rapid reversal of acidosis may impair
cardiac function, reduce tissue oxygenation, and promote hypokalemia. May cause cerebral edema.

However, in the presence of severe acidosis (arterial pH <7.0), the ADA advises bicarbonate (50 mmol
[meq/L] of sodium bicarbonate in 200 mL of sterile water with 10 meq/L KCl per hour for 2 h until the
pH is >7.0).
Hypophosphatemia may result from increased glucose usage, but randomized clinical trials have not demonstrated
that phosphate replacement is beneficial in DKA. If the serum phosphate is <0.32 mmol/L (1 mg/dL), then phosphate
supplement should be considered and the serum calcium monitored.

Hypomagnesemia may develop during DKA therapy and may also require supplementation.
Foremost is patient education about the symptoms of DKA, its precipitating factors, and the
management of diabetes during a concurrent illness. During illness or when oral intake is
compromised, patients should (1) frequently measure the capillary blood glucose; (2)v measure
urinar m
y ketones when the serum glucose is >13.7 mmol/L (250 mg/dL); (3) drink fluids to
maintain hydration; (4) continue or increase insulin; and (5) seek medical attention if dehydration,
persistent vomiting, or uncontrolled hyperglycemia develop
 COMPLICATIONS
• Cerebral edema
• Pulmonary edema
• Cardiac dysrhythmia
• Myocardial injury
• Hypoglycemia
• Hypokalemia
• Diabetic retinopathy
 PROGNOSIS
• 0.2-2% overall mortality seen in DKA
• Signs of poor prognosis – at the time of diagnosis -> deep coma, hypothermia, oliguria..
• Fetal mortality rate in pregnancy with DKA is 30%
• Most common cause of death in DKA is cerebral edema
 HYPERGLYCEMIC
HYPEROSMOLAR STATE
• Hyperglycemia induces an osmotic diuresis that leads to intravascular volume depletion, which is
exacerbated by inadequate fluid replacement .

• The absence of ketosis in HHS is not understood. Presumably, the insulin deficiency is only relative
and less severe than in DKA. Lower levels of counterregulatory hormones and free fatty acids have
been found in HHS than in DKA in some studies

• Marked hyperglycemia (plasma glucose may be >55.5 mmol/L [1000 mg/dL]), hyperosmolality
(>350 mosmol/L), and prerenal azotemia
• The prototypical patient with HHS is an elderly individual with type 2 DM, with a several-week history of polyuria,
weight loss, and diminished oral intake that culminates in mental confusion, lethargy, seizure, abnormal body
movements or coma.

• Mental status changes begin when the plasma osmolality rises to 320mosm/KgH2O and coma can develop at plasma
osmolality of 340 mosm/kgH2O .

• The physical examination reflects profound dehydration and hyperosmolality and reveals hypotension, tachycardia, and
altered mental status

• Absent symptoms are- nausea, vomiting, and abdominal pain and the Kussmaul respirations characteristic of DKA.

• 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 sought.
• Fluid replacement should initially stabilize the hemodynamic status of the patient (1–3 L of 0.9%
normal saline over the first 2–3 h).

• Because the fluid deficit in HHS is accumulated over a period of days to weeks, the rapidity of reversal
of the hyperosmolar state must balance the need for free water repletion with the risk that too rapid a
reversal may worsen neurologic function.

• If the serum sodium is >150 mmol/L (150 meq/L), 0.45% saline should be used.

• After hemodynamic stability is achieved, the IV fluid administration is directed at reversing the free
water deficit using hypotonic fluids (0.45% saline initially, then 5% dextrose in water [D5W]).

• The calculated free water deficit (which averages 9–10 L) should be reversed over the next 1–2 days
(infusion rates of 200–300 mL/h of hypotonic solution).
• Potassium repletion is usually necessary and should be dictated by repeated measurements of the
serum potassium. In patients taking diuretics, the potassium deficit can be quite large and may be
accompanied by magnesium deficiency.

• Hypophosphatemia may occur during therapy and can be improved by using KPO4 and beginning
nutrition.

• A reasonable regimen for HHS begins with an IV insulin bolus of 0.1 unit/kg followed by IV insulin at
a constant infusion rate of 0.1 unit/kg per hour. If the serum glucose does not fall, increase the insulin
infusion rate by twofold. However, the insulin requirement will be decreased as the hypertonic
condition is corrected,( because hypertonicity promotes insulin resistance )
THANK YOU