Diabetic Emergencies

Dr.Gireesh kumar.K.P
 Diabetic ketoacidosis
• Diabetic ketoacidosis (DKA) is a state of absolute or
relative insulin deficiency aggravated by
hyperglycemia, dehydration, and acidosis-producing
derangements in intermediary metabolism.
• The most common causes are infections, disruption of
insulin treatment, and new onset of diabetes.
• DKA is typically characterized by hyperglycemia over
300 mg/dL, low bicarbonate (<15 mEq/L), and acidosis
(pH <7.30) with ketonemia and ketonuria and marked
dehydration,
Triad of DKA

• Hyperglycemia
• Severe dehydration
• Hyperketonemia with Metabolic acidosis
Causes

• Infection, especially pneumonia, urinary tract infection,

and sepsis
• Inadequate insulin treatment or noncompliance
• Infarction (cerebral-stroke, coronary-MI)
• Pregnancy and alcohol ingestion.
Dehydration = DKA
Clinical features of diabetic ketoacidosis

Symptoms Signs
Polyuria, Dehydration Hypotension - Hypotension indicates
thirst a loss of >10% of body fluids.
Weight loss Cold extremities/peripheral cyanosis
Weakness Tachycardia
Nausea, Air hunger (Kussmaul breathing)
vomiting Smell of acetone
Leg cramps Hypothermia
Blurred vision Confusion,
Abdominal pain drowsiness,
coma (10%)
Deficits in diabetic ketoacidosis
• Fluid deficit : 6 L(100 mL / kg body weight)
– 3 liters extracellular - replace with normal saline
– 3 liters intracellular - replace with dextrose
• Sodium deficit : 7 to 10 mEq / kg body weight
• Potassium deficit : 3 to 5 mEq / kg
• Phosphate deficit : 5-7 mEq / kg
• Magnesium deficit : 1-2 mEq / kg
• Calcium deficit : 1-2 mEq / kg
Labs

• Urea – elevated due to dehydration or renal failure

• Creatinine – elevated in renal failure (pre renal failure due to dehydration)
• Sodium: sodium is reduced as a consequence of the hyperglycemia [1.6 meq
reduction in serum sodium for each 100 mg/dL rise in the serum glucose]. A
normal serum sodium in the setting of DKA indicates a more profound water
deficit.
• Serum osmolality [ 2 (Na + K+) + Glucose + Urea (all in mmol) ] is mildly to
moderately elevated, though to a lesser degree than that found in HHS
• WBC – Elevated in sepsis/infections
• ECG –To rule out myocardial infarction, Hypokalemia, Hyperkalemia
• Infection screen
Labs
• Ketone bodies - urine and blood for ketones
– Serial serum ketone test is not needed, because ketonemia
lags behind clinical recovery; closure of the anion gap is a
more reliable index of metabolic recovery.
• ABG - arterial blood gases to assess the severity of
acidosis ( high anion gap acidosis *) ,
– Repeat arterial blood gases are unnecessary during the
treatment of DKA; [ venous pH, which is about 0.03 units lower
than arterial pH is adequate to assess the response to therapy
].
Fluids
• In diabetic ketoacidosis, the initial treatment of choice is rehydration, typically with a 0.9 %
saline administered at a rate of 7 to 14 mL / kg / hour.
• Normal saline / 0.9% saline i.v.
– 1 litre in first 30 minutes
– 1 litre over next 1 hr
– 1 litre over next 2 hrs
– 1 litre over next 2-4 hrs
– Half normal saline(0.45%) infused at 4 to 14 mL/kg per hour is appropriate if the corrected serum
sodium is normal or elevated.
• This also increases insulin responsiveness by lowering the plasma osmolality (Posm),
reducing vasoconstriction and improving perfusion, and reducing stress hormone levels
• When blood sugar drops to 250 mg/dl
– Start 5% dextrose, 1 litre 8-hourly
– If still dehydrated, continue 0.9% saline and add 5% dextrose 1 litre per 12 hrs
– Rapid drop of sugars may lead to brain oedema * especially in children
– Management of cerebral oedema – 3% saline ,Mannitol , Hyperventilation
Fluids
• Typical fluid requirement is 6 liters in first day
• Subsequent fluid replacement should be based on clinical
response and urine output
• Fluid infusion is continued until the fluid intake/output
records indicate a positive fluid balance
• Monitor for fluid overload in elderly and cardiac failure
patients (JVP, pulmonary oedema - lung crepitations)
• Serum sodium can increase as hyperglycemia is
corrected; failure to see this suggests that the patient is
fluid overloaded with free water.
Insulin
• Start low-dose (IV regular insulin and rapid-acting insulin analogs are
equally effective in treating DKA)
• Initial IV infusion of 0.15 unit / kg regular insulin (or
10units) followed by the continuous IV infusion of regular
insulin prepared in normal saline 0.1U/Kg/hr.
• A decrease in blood sugar of 50 - 75 mg/dL/hr is an appropriate response
• 6 units/hr infusion initially: Divide initial BG level by 100, then round to nearest 0.5 units for
bolus AND initial infusion rate.
• Example: Initial BG = 625 mg/dL: 625 ÷ 100 = 6.25, round ↑ to 6.5
– 5 units/hr when blood sugar <500 mg/dl
– 4 units/hr when blood sugar< 400 mg/dl
– 3 units/hr when blood sugar< 300 mg/dl
– 2 units/hr when blood sugar< 200 mg/dl
– Then maintain at 0.05–0.1 units/kg per hour infusion.
Insulin
• If initial serum potassium is < 3.3 meq/L, do not administer insulin until the
potassium is corrected to > 3.3 meq/L (worsen the hypokalemia by driving
potassium into the cells)
• Measure glucose every 1–2 h; measure electrolytes (especially K+,
bicarbonate, phosphate) and anion gap every 4 h for first 24 h.
• Monitor blood pressure, pulse, oxygen saturation, mental status, fluid intake
and output every 1–4 h.
• Continue above until patient is stable, Sugars 150–250 mg/dL, and acidosis
is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour
to prevent dangerous hypoglycemia.
• Administer intermediate or long-acting insulin as soon as patient start eating.
• Allow overlapping of insulin infusion and subcutaneous insulin injection, give
the first SC injection of insulin approximately 30 minutes before
stopping the IV route.
Intravenous insulin analogs? — There is no reason to use rapid-acting analogs
in IV insulin therapy since the kinetics are identical and the data do not show any important
advantage.

• The use of IV insulin preparations other than regular insulin was evaluated in a study of 74
patients with DKA who were randomly assigned to IV regular or glulisine insulin [22]. The
initial dosing was the same in both groups (0.1 unit/kg IV bolus, followed by an infusion at 0.1
unit/kg per hour). Patients were otherwise treated similarly, according to ADA guidelines.
After resolution of DKA, patients treated with regular insulin received subcutaneous NPH and
regular insulin twice daily, whereas patients treated with IV glulisine insulin received glargine
once daily and glulisine before meals. There were no differences between the two groups in
the mean duration of treatment, amount of insulin administered, or duration of insulin infusion
until resolution of DKA. After transition to subcutaneous insulin, glycemic control was also
similar. However, patients treated with NPH and regular insulin had a higher incidence of
hypoglycemia. Thus, IV regular and glulisine insulins were equally effective in treating DKA.
• TI :Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial.
• AU:Umpierrez GE, Jones S, Smiley D, Mulligan P, Keyler T, Temponi A, Semakula C, Umpierrez D, Peng L, Cerón M, Robalino G
• SO:Diabetes Care. 2009;32(7):1164. Epub 2009 Apr 14.
Subcutaneous insulin in DKA?
• Subcutaneous insulin — Patients with mild DKA can be safely treated with
subcutaneous, rapid-acting insulin analogs on a general medical floor or in the
emergency department but only when adequate staffing is available to carefully monitor the
patient and check capillary blood glucose with a reliable glucose meter every hour. The initial
dose of the rapid-acting insulin analog is 0.3 units/kg, followed by hourly injections of 0.1
units/kg until resolution of hyperglycemia and ketoacidosis.
• Direct comparison of intramuscular, subcutaneous, and IV insulin therapy for
hemodynamically stable DKA patients shows similar efficacy and safety [1-2]. In
addition, subcutaneous administration of rapid-acting insulin analogs (insulin lispro, aspart,
and glulisine) in the management of uncomplicated DKA has been demonstrated to be safe
and cost effective in two randomized trials in adults [31,32]. In one trial, for example, 40
patients with DKA were assigned to one of two regimens

• TI:Diabetic ketoacidosis: low-dose insulin therapy by various routes.

• AU:Fisher JN, Shahshahani MN, Kitabchi AE
• SO:N Engl J Med. 1977;297(5):238.
• TI:Treatment of diabetic ketoacidosis with subcutaneous insulin aspart.
• AU:mpierrez GE, Cuervo R, Karabell A, Latif K, Freire AX, Kitabchi AE
• SO:Diabetes Care. 2004;27(8):1873.
Potassium
• If serum potassium < 3.5 meq/L, give 40 mEq/L added
potassium
– Give in 1 litre of fluid (NS)
– Avoid infusion rate of > 20 mEq/hr
• If serum potassium is 3.5-5.0 meq/L, give 20 mEq added
potassium
• If serum potassium is > 5.0 mEq/L , or patient is anuric,
potassium is not required
• The serum potassium should be maintained 4.0 - 5.0
meq/L.
Bicarbonate
• Its use is controversial
– In a randomized trial of 21 DKA patients with an admission arterial pH between 6.90 and 7.14
(mean 7.01), bicarbonate therapy did not change morbidity or mortality [*].
• However, bicarbonate therapy may be useful and should be considered for
DKA patients with
– Shock or coma,
– Severe acidosis (pH < 7.0),
– Acidosis-induced cardiac or respiratory dysfunction,
– Severe hyperkalemia.
• Administer 100 meq of sodium bicarbonate in 400 mL NS with 20 meq of
potassium chloride, if the serum potassium is less than 5.3 meq/L,
administered over two hours.
– The venous pH should be monitored every two hours, and infuse bicarbonate as
above, until the pH > 7.00.
– Complete correction of the acidosis should not be attempted.
Supportive therapy

• Catheterisation ( if no urine passed after 3 hrs)

• Nasogastric tube to keep stomach empty in patients with
impaired consciousness
• Central venous line to monitor CVP – if associated
cardiac failure
• Plasma expander if systolic BP is < 90 mmHg or does not
rise with i.v. saline
• Antibiotics if infection is suspected
• Magnesium and phosphate correction if needed.
Complications of DKA
• Lactic acidosis due to prolonged dehydration, infection, shock, and tissue
hypoxia in DKA patients.
• Lactic acidosis should be suspected in refractory metabolic acidosis and a
persistent anion gap despite optimal therapy for DKA.
• Acute respiratory distress syndrome (ARDS)
• Arterial thrombosis manifesting as stroke, myocardial infarction, or an
ischemic limb
• Venous Thromboembolism
• Disseminated intravascular coagulation (rare)
• Acute circulatory failure / shock
• Rebound ketoacidosis can occur due to premature cessation of insulin
therapy.
DKA Vs HHS
DKA Hyperosmolar state

Blood sugar (mg/dl) 250 to 600 600 to 1200

Average fluid deficit 6 liters in first day 9 to 10 Liters

Serum Sodium (mEq/L) 125 to 135 135 to 145 ( or > 145)

Blood Urea, Creatinine Mild Increase Moderate increase

Serum Osmolality 300 to 320 330 to 380

Plasma Ketones ++++ -/+

Serum Bicarbonates Low Normal

Blood pH Low(acidosis) Normal

Anion gap High anion gap Normal

Insulin requirement High Low

Plasma osmolality = 2 (Na+) + 2 (K+) + Glucose + Urea (all in mmol)

Switching of insulin to SC

• The American Diabetes Association (ADA) guidelines for DKA recommend

that IV insulin infusion be tapered and a multiple-dose, subcutaneous insulin
schedule be started when the blood glucose is <200 mg/dL (11.1 mmol/L)
and at least two of the following goals are met [1]:

– Serum anion gap <12 mEq/L (or at the upper limit of normal for the local laboratory)
– Serum bicarbonate ≥15 mEq/L
– Venous pH >7.30
Thank U