Diabetic emergencies

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Emergencies in Diabetes
  • Hypolglycaemia
  • Diabetic ketoacidosis
  • Hyperosmolar hyperglycemic state - HHS ( hyperosmotic hyperglycaemic Non ketotic state)
  • The overall mortality recorded among children and adults with DKA is <1%.
  • Mortality among patients with HHS is ∼10-fold higher than that associated with DKA.
Hypoglycaemia
Hypoglycaemia is defined as blood glucose < 72 mg/dL (4 mmol/L). Any patient with blood glucose < 72 mg/dL (4 mmol/L) with or without symptoms should be treated with 15 – 20 grams of quick acting carbohydrate as soon as hypoglycaemia is diagnosed.
Symptoms
—Neurogylycopaenia
—-confusion
—-agitation
—-dysarthria
—-focal neurological deficits
—-seizures
—-coma
—Adrenergic symptoms
—-palpitations
—-sweating
—-tremor
Causes of hypoglycaemia
Drugs - insulin,
oral hypoglycemic agents
aspirin
beta-blockers
Liver disease (e.g., hepatitis, hepatoma, acetaminophen overdose
Alcohol
Infection
Pituitary dysfunction
Adrenal insufficiency
Insulinoma
Neoplasm
Management
—cooperative conscious able to swallow
—-25% dextrose 75 ml orally
—uncooperative semi /un conscious unable to swallow
—-25% dextrose 75ml or
—-10% dextrose 150-200ml over 15 min
—Followed by a subsequent intravenous infusion of 10% glucose at infusion rate 100ml/hr
—subcutaneous or intramuscular injection of 0.5 to 1.0 mg of glucagon
—Regular CBS monitoring for 24 to 48 hrs
—If able to take orally start on carbohydrate containing meal
—Review insulin /hypoglycaemic drug regimen
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Guidelines
The type of carbohydrate and the route of administration depend on the patient’s level of consciousness, ability to swallow and the need to keep the patient nil by mouth as described by the following algorithm
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Patients who experience hypoglycaemic symptoms but have a blood glucose level >72 mg/dL should be treated with a small carbohydrate snack only.
The following key points are important in management of hypoglycaemia
  • Use oral glucose when possible to avoid complications of IV glucose administration and to maintain a smoother glycaemic control. - Avoid using 50% dextrose. It is highly irritant and can cause serious complications. (severe thrombophlebitis and subsequent infection)
  • Use a large bore cannula in a large vein when using IV dextrose
  • If IV access is not available glucagon im can be given, if available.
  • Do not omit next insulin or oral hypoglycaemic dose, but review the dose
Further Assessment: 
Look for a cause for hypoglycaemia and correct it
o Erratic behavior – Incorrect dose/ technique, alcohol, vigorous exercises, skipping meals
o Complication of diabetes –Renal impairment, autonomic neuropathy & hypoglycaemia unawareness
o Other – Adrenal insufficiency
In the presence of hypoglycaemia unawareness or episode of severe hypoglycaemia:
o Re-evaluate treatment regimen o Insulin-treated patients: raise glycemic targets for several weeks to partially reverse hypoglycaemia unawareness and reduce recurrence
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is an acute life-threatening complication of diabetes. It occurs mainly in patients with Type 1 DM. However, DKA can complicate Type 2 DM as well. DKA is a complex disorder of metabolic state characterized by hyperglycaemia, ketoacidosis, and ketonuria due to relative or absolute insulin deficiency.
Precipating factors
—Poor compliance with the insulin regimen
—New onset type 1 diabetes, in which DKA is a common presentation
—Acute major illnesses such as infection, myocardial infarction, cerebrovascular accident, or pancreatitis.
—pregnancy
—Medications
—glucocorticoids
—Sodium glucose cotransporter (SGLT) inhibitors
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Clinical presentation
—Abdominal pain with vomiting
—Volume depletion with circulatory collapse
—decreased skin turgor, dry axillae and oral mucosa, low jugular venous pressure, increased capillary refilling time, tachycardia and, if severe, hypotension
—Labored respiration
—Fruity odor due to acidosis
—Decreased sensorium
Initial Evaluation
  • Airway, breathing, and (ABC) status
  • Mental status
  • Circulation/ Volume status
  • Possible precipitating events (eg, source of infection, myocardial infarction)
Diagnosis
  • Ketonaemia > 3.0 mmol/L or significant ketonuria (more than 2+ on standard urine sticks)
  • Blood glucose > 11.0mmol/L (200 mg/dL) or known diabetes mellitus
  • Bicarbonate < 15.0mmol/L and/or venous pH < 7.3
—(ABG only if patient has a reduced conscious level or low oxygen saturations)
Labs
  • Serum glucose
  • Serum electrolytes (with calculation of the anion gap), BUN, and serum creatinine
  • Complete blood count with differential
  • Urinalysis, and urine ketones by dipstick
  • Plasma osmolarity Measure or calculate
  • plasma osmolarity = 2 (Na + K) + BUN/3 + glucose/18.
  • Serum ketones (if urine ketones are present)
  • Venous / Arterial blood gas
  • Electrocardiogram
  • FBC
  • Amylase and lipase levels
Addiotional investigations
—cultures of
—urine,
—Blood
— serum lipase and amylase
—Acute pancreatitis
—causes – alcohol, hypertriglyceridemia
—chest x-ray,
—U/S scan abdomen
—Hb A1 C
—CT abdomen
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Assessment of severity
The presence of one or more of the following may indicate severe DKA and should be reviewed by specialist and considered for referral to a HDU (High Dependency Unit) care
  • Bicarbonate level below 5 mmol/L
  • Venous/arterial pH below 7.0
  • Blood ketones over 6 mmol/L
  • Hypokalaemia on admission (under 3.5mmol/L)
  • GCS less than 12
  • Oxygen saturation below 92% on air (assuming normal baseline respiratory function)
  • Systolic BP below 90mmHg
  • Pulse over 100 or below 60bpm
• Anion gap above 16 [Anion Gap = (Na+ + K+) – (Cl- + HCO3-)
Management
—Correction of fluid loss with intravenous fluids
—Correction of hyperglycemia with insulin
—Clearance of ketones and Suppression of ketogenesis
—Correction of electrolyte disturbances, particularly potassium deficit
—Correction of acid-base balance
—Treatment of any comorbidity
—--Infection / MI / CVA
Typical deficits in DKA
—Water 100 ml/kg ( for 50 kg person 5 liters)
—Sodium 7-10 mmol/kg (for 50 kg person 500 m mol)
—Chloride 3-5mmol/kg
—Potassium 3 mmol/kg
1) Fluid replacement
Assess the severity of dehydration clinically by pulse and blood pressure. If systolic BP (SBP) on admission is below 90mmHg consider other causes of low blood pressure such as cardiogenic shock and sepsis in addition to hypovoalemia.
• Give 500ml of 0.9% sodium chloride solution over 10-15 minutes.
  • If SBP remains below 90mmHg this can be repeated
• If there has been no clinical improvement reconsider other causes of hypotension and seek an immediate specialized assessment
  • Once SBP above 90mmHg continue fluid replacement as shown in Table 14.
—Rehydration : Normal saline
1000 ml over 1 st hour
1000 ml over next 2 hours
—Subsequent infusion rates depend of the state of hydration/ UOP/ BP
—exercise caution in the following patients
ØYoung people aged 18-25 years
ØElderly
ØPregnant
ØHeart or kidney failure
ØOther serious co-morbidities
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Exercise caution and use central venous pressure measurements where possible to guide the rate of fluid administration in following groups of patients
  • Young adults aged <25 years
  • Elderly
  • Pregnant
• Heart or kidney failure
  • Other serious co-morbidities
When blood glucose falls below 250 mg/dl (14.0 mmol/L), commence 10% glucose given at 125ml/hour alongside the 0.9% sodium chloride solution
2) Insulin therapy
Fixed Rate Intravenous Insulin Infusion (FRIII) via infusion pump dose 0.1 units/kg/hour
Regular insulin /Soluble insulin /Human insulin via pump at a rate of 6-12 units /hour
((If syringe pump not available administer insulin IM ( 0.1 unit / kg )))
—
When blood sugar around 200 switch S/C insulin tds dose adjusted according to blood sugar
When patient is able to take orally a fixed dose insulin regimen may be more appropriate
Intravenous insulin infusion of 0.1 units/per kilogram body weight is recommended
Monitor capillary blood glucose hourly
Metabolic treatment targets:
• Reduction of the blood ketone concentration by 0.5mmol/L/hour
  • Increase the venous bicarbonate by 3.0mmol/L/hour
• Reduce capillary blood glucose by 3.0mmol/L/hour
  • Maintain potassium between 4.0 and 5.5mmol/L
If these rates are not achieved, then the rate of insulin infusion should be increased
Continue insulin infusion until the ketone measurement is less than 0.6mmol/L, venous pH over 7.3 and/or venous bicarbonate over 18mmol/L (Resolution of DKA)
3) Potassium replacement
Although DKA patients may present with hyperkaelemia, with treatment (Fluid and insulin) potassium level falls. Table 15 will give a guide to potassium replacement
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—K supplementation may be necessary as extracellular K moves into cells rapidly with infusion of insulin.
—Aim is to maintain k between 4 -5.5 mEq/L
K > 5.5 Nil
K = 3.5- 5.5 add 40 mmol /l of infusion solution
—Measure potassium 2 hourly
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4) Correction of acidosis
Fluid and insulin replacement usually corrects acidosis. Bicarbonate administrations is potentially dangerous and not recommended.
—Initially HCO3 for correction of academia is usually not necessary unless the patient has impending cardiac arrest
—If academia persists after correction of volume deficit and hyperglycemia a HCO3 infusion may be given.
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5) Assessment of resolution of ketoacidosis
  • Blood ketones less than 0.6mmol/L and
• Venous pH over 7.3 (do not use bicarbonate as a surrogate at this stage because the hyperchloraemic acidosis associated with large volumes of 0.9% sodium chloride will lower bicarbonate levels)
6) Other key strategies (adjuvant therapy)
  • Identify and treat precipitating factors Infections, other stresses include pancreatitis, myocardial infarction, stroke, trauma, and alcohol and drug abuse • Prophylaxis for DVT
— low molecular weight heparin
—infection – broad spectrum IV antibi0tics
—Ketosis persist even after blood sugar < 250 infusion of dextrose and insulin may be necessary until all ketones disappear from the urine/blood
7) Conversion to subcutaneous insulin
Intravenous Insulin infusion should be converted to an appropriate subcutaneous regimen when DKA is resolved and the patient is ready and able to eat.
Intravenous insulin infusion should not be discontinued for at least 30 to 60 minutes after the administration of the subcutaneous dose is given with a meal
  • Restarting subcutaneous insulin for patients already established on insulin The patient’s previous regimen should generally be re-started if their most recent HbA1c suggests acceptable level of control i.e. HbA1c <8.0%
  • Calculating the subcutaneous insulin dose in insulin-naïve patients Estimate Total Daily Dose (TDD) of insulin = patient’s weight x 0.5 or 0.75. (Use 0.75 units/kg for those thought to be more insulin resistant i.e. teens, obese) Calculate Basal Bolus (QDS) Regimen or twice daily (BD) regimen
MONITORING OF PATIENT IN DKA
—Monitoring of vital signs with patient linked to a multi para monitor
—Continuous pulse oximetry
—Fluid balance chart
with bladder catheterization if required
maintain UOP > 0.5ml/kg/hour
—Blood glucose hourly Capillary BS
—Blood ketones in blood hourly
—Venous blood gas at 1 hour and then 2 hourly for
pH / bicarbonate
—Serum electrolytes (laboratory) – 4 hourly
—Assess for complications
COMPLICATIONS ASSOCIATED WITH DKA
—Cerebral oedema
—CVT
—Acute coronary syndome
—DVT
—Acute gastric dilatation
—Erosive gastritis
—Late hypoglycemia
—Pulmonary oedema
—Infection (most commonly, urinary tract infections)
—Acute kidney injury
—Mucormycosis
—Cerebrovascular accident
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Hyperosmolar hyperglycaemic states (HHS)
Hyperosmolar hyperglycemic state is a life threatening metabolic derangement that occur mostly in patients with type 2 DM who have some concomitant illness that leads to reduced fluid intake. Infection is the most common preceding illness and it is usually present in older patients with type 2 DM. HHS carries a higher mortality than DKA
—Usually the blood sugars are very high > 600 mg /dl
— pH is greater than > 7.3
—serum bicarbonate > 15 mEq/L.
—ketonaemia (<3.0mmol/L)
—Measured as Beta-Hydroxybutyrate
—Dehydration is more sever
—Osmalarity > 320
—More fluid necessary initially
—Insulin requirement is less as there are no ketone bodies
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DIagnosis
  • Hypovolaemia
  • Marked hyperglycaemia (30 mmol/L or more) without significant ketonaemia (<3 mmol/L) or acidosis (pH>7.3, bicarbonate >15 mmol/L) • Osmolality > 320 mOsm/kg Alteration in mental status is common if osmolality> 330 mOsm/kg
Management
Fluid replacement
Fluid losses in HHS are estimated to be between 100 -220 ml/kg (6 -13 liters in a 60 kg person) with Na+ loss (300 -780 mmol), K+ loss (240 -360 mmol/L) and Clloss (300 -900mmol)
The aim of treatment should be to replace approximately 50% of estimated fluid loss within the first 12 hours and the remainder in the following 12 hours
Use 0.9% sodium chloride solution to restore circulating volume and reverse dehydration. Fluid replacement alone will lower blood glucose, serum sodium and osmolality
Rapid changes must be avoided – a safe rate of fall of plasma glucose of between 4 and 6 mmol/h is recommended
Measure or calculate osmolality every hour initially and the rate of fluid replacement should be adjusted to ensure a positive fluid balance sufficient to promote a gradual decline in osmolality.
The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours
If osmolality is no longer declining despite adequate fluid replacement with 0.9% saline AND an adequate rate of fall of plasma glucose, 0.45% sodium chloride solution should be substituted
Insulin therapy
Insulin should not be started before fluid resuscitation unless there is significant ketonemia (clinical or 3β-hydroxy butyrate > 1 mmol/L)
The recommended insulin dose is intravenous insulin infusion given at 0.05 units per kg per hour.
A fall of glucose at a rate of up to 5 mmol/L per hour is ideal Once the blood glucose has ceased to fall following initial fluid resuscitation, insulin may be started or, if already in place, the infusion rate increased by 1 unit/hr.
Potassium therapy
Hyperkaelemia and Hypokaelemiais less common than in DKA. If serum K is between 3.5 mmol/L to 5.5 mmol/L, replacement should be done with 40 mmol of KCl and if serum K >5.5 mmol/L, no replacement is indicated.
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Recovery phase
Complete correction of electrolyte and osmolality abnormalities is unlikely to be achieved within 24 hours and too rapid correction may be harmful. Early mobilization is recommended. Intravenous insulin infusion can usually be discontinued and subcutaneous insulin can be started once patient is able to eat and drink but IV fluids may be required for longer if intake is inadequate. For patients with previously undiagnosed diabetes or well controlled patients on oral agents, switching from insulin to the appropriate oral hypoglycaemic agent should be considered after a period of stability (weeks or months)
Random case study
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Gkucogin not avaible Sri Lanka's
Should keep monitoring because effect of overdose still there
Acute adrenal I suff and DKA can mimick abdominal pain and oancretatitis
Arterial blood has vs venous blood gas. Venous blood gas sufficient.
Mcq points important? Like deficit of fluids in DKA? Do pps and have idea of what important.
Na lost because of diuresis.. Water and NA lost together
...
Young adults fluid precautions because can lead to pulmonary oedema
Human insulin usually used...
Insulin.. Human insulin though fixed rate pump or syngrine pump.. If not avakibel then soluble insulin IM...it will act like a depot and give slowly..cant give IV because low half life.... And cant give SC because too slow.. Depot formation...
IV faster than I'm faster than SC
Types of insulin? Clarify again
ECG changes in potassium disorders
Rare instance of giving both destrose and insulin. 1. For hyoerkalemia 2 to get rid of ketone bodies...
What about the guidelines stuff?
Guidelines... Lecture... Textbook.... Research other stuff