This is a ppt presentation regarding Acute Hyperglycemic Emergencies we face in routine clinical practices and their management from Harrison's Principles of Medicine and Paul Marino Emergency Management book By Dr.V.B.Kasyapa. J (MD GM)

1. Acute hyperglycemiC emergencies
Dr. V. B. Kasyapa. J
GM PG I year

2. Severe Hyperglycaemia
• In a Type 1 or 2 DM patient,
– Blood glucose > 16.7 mmol/L [>300 mg/dL]
• It can be manifested as,
– Diabetic Keto Acidosis (DKA)
– Hyperglycaemic Hyperosmolar State (HHS)
• These two entities are a part of disease
continuum, with or without ketonemia

3. • Commonly characterised by,
– Absent/ relative insulin deficiency
– Volume depletion
– Acid base abnormality
• Usually precipitated,
– Infections
– Infarcts
– Other comorbidities

4. DKA – Presentation
• Symptoms may develop over 24 hrs
• May be seen in established diabetes or in a
type 1 DM, as the presenting feature
• Nausea & Vomiting (most prominent)
• Abdominal pain (resembles acute abdomen)
• Cerebral edema (most commonly seen in
children)

5. • Increased serum glucose causing,
– Glusosuria
• Osmotic diuresis
– Fruity odor
– Volume depletion
• Hypotension
• Lethargy
• Altered mentation

7. Precipitating factors
• Inadequate insulin administration
– By patient
– By health care personnel
– By brief interruption during short acting insulin delivery
– Due to eating disorders
• Infections (pneumonia/ UTI/ GE/ Sepsis)
• Infarction (cerebral/ coronary/ mesenteric/ peripheral)
• Drugs (Cocaine, etc)
• Pregnancy

8. Pathology
Relative/absolute
deficiency of insulin
↓ PFK & F 1,6-
BisPhosphatase
↓ F 2,6-
BisPhosphate
↓ glycolysis
↑ PEP carboxylase
↑ gluconeogenesis
↓ GLUT 4 receptors
in skeletal muscle &
fat
↓ glucose uptake
by skeletal muscle
Anaerobic
respiration ↑
forming Lactic
acidosis
↓ intracellular
utilisation of
glucose by adipose
tissue
↓ insulin sensitive
lipoprotein lipase
↓ VLDL utilisation
by periphery

9. Excess of counter
regulatory
hormones
↑
catacholemines,
GH
↑ lipolysis
↑ FFA converted
to TGA & VLDL
Autonimic
disturbances
Hypotension
Peripheral
vasodilatation
↑ glucogon
↑ glycogenolysis
↑
gluconeogenesis
↑ ketone body
synthesis (↑
carnitine palmitoyl
transferase)
Beta hydroxy
butyrate (high
amounts & first
line)
Acetoacetate
(Mostly seen)
acetone

10. • At physiological pH
– Ketone bodies  ketoacids (neutralised by HCO3)
• As HCO3 depletes
– Ketoacidosis
• Excess inflammatory cytokines
– Elevated ESR, CRP
– Abdominal pain
– SIRS

11. Lab diagnostics
• Serum glucose
– Moderate to marked elevation
– Sometimes may be below 300 mg/dL
• Serum HCO3
– Usually <10 mmol/L
• Arterial pH
– 6.8 to 7.3 depending upon severity

12. • Potassium
– Total body deficit always present
– d/t acidosis near normal or elevated serum levels
can be seen
• Other electrolytes (Na, P, Cl & Mg)
– Total body deficit
– d/t hypovolemia and hyperglycaemia near normal
levels are seen
– For every 100mg/dL glucose rise there will be 1.6
mEq Na fall in serum is seen
– So, normal serum Na levels indicate dehydration

13. • ↑ BUN d/t hypovolemia
• ↑ Serum creatinine d/t hypovolemia &
interference by acetoacetate in blood tests
• ↑ Lipid profile (TGA, VLDL)
• ↑ Amylase
– Often salivary
– Pancreatic amylase elevated in acute pancreatitis
• ↑ Serum lipase in acute pancreatitis
(confirmation)

14. • ↑ osmolarity but lesser when compared to HHS
• Ketone bodies
– Preferred diagnosis by blood Beta Hydroxybutyrate
– Normally seen is Acetoaetate in urine by nitroprusside
dipsticks
– These may give false positive values in captopril &
penicillamine intake
• Blood glucose levels will not always correlate with
metabolic acidosis
• Mild to severe metabolic acidosis with High
Anion-Gap is present

15. Anion-Gap
• In a metabolic acidosis patient
AG = Na – (Cl + HCO3)
Albumin corrected AG = AG + [2.5 x (4.5 – serum
albumin)]
Normal values 8-10 mEq/L
– To detect underlying acid base deformity
Gap-Gap ratio = (AG excess)/(HCO3 Deficit)
= (AG – 10)/(24 – S.HCO3)

16. • In high AG metabolic acidosis
– GG ratio > 1 (more HCO3 deficit)
• Coexisting hyperchloremic metabolic acidosis
– D/t saline infusion in DKA treatment
– GG ratio = 1
• Pure DKA
– GG ratio < 1 (alkali is added)
• Coexisting metabolic alkalosis
– Uremia with vomiting
– DKA with continuous ryles aspiration/ diuretics

17. DD
• Alcoholic acidosis ( >15 mmol/L HCO3)
• Starvation acidosis
• Toxins

18. TREATMENT

21. Treatment
• Comprehensive flow sheet maintenance
– Vitals
– Input- Output
– Test values
– Treatment
• Fluid replacement
– Change to 0.45% NS after initial 0.9% NS bolus infusions or
initiate with RL to prevent hyperchloremia

22. • Insulin management
– IV insulin is preferred
– In mild cases
• Short acting SC insulin frequent dosing
– IV insulin should be continued until the resolution
of acidosis and ketosis, not merely glucose levels
• Till oral feeds started
• Then half the dose and add long acting SC insulin
according carbohydrate intake

23. • Hyperglycemia improvement
– Acutely, in first 1-2 hrs of treatment,
• Rapid improvement d/t volume replenishment
– Later on
• 75 – 100 mg/dL per hour
• d/t insulin mediated glucose disposal, Decreased hepatic
glucose production, rehydration
– So when 250 mg/dL achieved
• Add 5% glucose to 0.45%NS infusion
• Along with half the IV insulin infusion dose

24. • Ketosis resolution
– ↓ lipolysis
– ↑ peripheral use
– ↓ hepatic production
– ↑ HCO3 regeneration
– BHB converts to Acetoacetate (initial increase in ketone bodies
in nitroprusside based tests)
• Acidosis improvement
– Primarily by hyperchloremia (d/t treatment)
– Principally by Kidney replanishing the HCO3 stores and excreting
chlorine

25. • Hypokalemia during treatment
– Insulin mediated uptake
– Resolution of acidosis
– Urinary loss of potassium salts & organic acids
– Start potassium replacement when urine output is achieved
• HCO3 replacement
– Not necessary, as rapid correction worsens CNS status
– In severe acidosis (<7.0)
• [50mmol NaHCO3 + 200ml sterile water + 10 mmol KCl] per hour for 2
hrs until pH>7

26. • Phosphate and Magnesium replacement
• Only if severe, not routine
• Phosphorous serum level <0.5 mg/dL
0.5 mmol/kg IV infused over 4-6 hr
• Magnesium serum level <0.8mEq/L;
supplements should be given

27. Prognosis
• Mortality (<1%) with early recognition and
prompt treatment
• Often depends on underlying/ precipitating event
severity
• Major non-metabolic complication is Cerebral
edema, most common in children
– No guidelines but avoid over correction of water loss

28. Follow up
• Patient education,
– Symptoms
– Precipitating factors
– Management of concurrent illness
• Patient during illness/ compromised oral intake
– Frequent capillary glucose check up
– If >300 mg/dL, go for urine ketone bodies
– Drink lots of oral fluids
– Continue or increase the insulin
– Seek medical attention

29. HHS
• Common in elderly type 2
• Several weeks of polyuria, weight loss & D oral
intake present, which leads to CNS depression
• Profound, chronic dehydration is the rule
• Absent,
– Nausea, vomiting, abdominal pain & kussumaul
respiration

30. • Precipitating factors
– Stroke
– Sepsis
– Pneumonia
– Debilitating disorders
– Dementia
– Social situations compromising water intake

31. Pathology
• Relative insulin deficiency,
– ↑ hepatic glucose production by glycogenolysis
– ↓ glucose utilisation in periphery
• Inadequate fluid intake
• Hyperglycaemia
• Lower levels of counter regulatory hormones and
FFA, when compared to DKA

32. Lab diagnostics
• Marked hyperglycemia
– Often > 55.5 mmol/L ( > 1000 mg/dL)
• Hyper osmolarity (> 350 mOsm/L)
• Pre renal azotaemia
• Sodium
– Total body deficit,
– Normal or slightly low serum values even with marked
hyperglycemia
• Corrected Na = 1.6 mEq/100 mg/dL rise of serum
glucose + Serum Na

33. • No ketosis/ acidosis
– Small anion gap acidosis may be with lactic
acidosis
– Moderate ketonemia if associated starvation

34. Treatment
• Frequent monitoring is crucial
• Correct the underlying conditions
• Fluid replacement,
– Till hemodynamically unstable
• 1-3 L 0.9% NS over 2-3 hrs (avoid rapid correction)
• If Serum Na >150 mEq/L; use 0.45% NS
– After hemodynamic stability
• Calculated water deficit will be around 9-10 L
• Correct it in 2-3 days @ 200-300 ml/hr
• Use 0.45% NS

35. • Potassium replacement as necessary;
if associated with diuretic intake correct Magnesium also
• Insulin therapy,
– 0.1U/kg IV bolus
– 0.1 U/Kg/hr IV infusion
– Double; if no fall in 1 hr
– Add 5% glucose to half dose infusion; when serum glucose <250 mg/dL
– Continue until oral feeding started
– SC insulin should be started with long acting insulin according carbohydrate
intake
– Discharge with insulin
– At later date change to oral hypoglycemic drugs

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