Acute hyperglycemiC emergencies

Dr. V. B. Kasyapa. JGM PG I year

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

• Commonly characterised by,– Absent/ relative insulin deficiency– Volume depletion– Acid base abnormality

• Usually precipitated,– Infections– Infarcts – Other comorbidities

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)

• Increased serum glucose causing,– Glusosuria• Osmotic diuresis

– Fruity odor– Volume depletion• Hypotension• Lethargy• Altered mentation

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

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

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

• At physiological pH

– Ketone bodies ketoacids (neutralised by HCO3)

• As HCO3 depletes

– Ketoacidosis

• Excess inflammatory cytokines

– Elevated ESR, CRP

– Abdominal pain

– SIRS

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

• 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

• ↑ 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)

• ↑ 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

Anion-Gap

• In a metabolic acidosis patientAG = 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)

• 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

DD

• Alcoholic acidosis ( >15 mmol/L HCO3)

• Starvation acidosis

• Toxins

TREATMENT

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

• 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

• 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

• 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

• 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

• 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

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

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

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

• Precipitating factors

– Stroke

– Sepsis

– Pneumonia

– Debilitating disorders

– Dementia

– Social situations compromising water intake

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

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

• No ketosis/ acidosis

– Small anion gap acidosis may be with lactic

acidosis

– Moderate ketonemia if associated starvation

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

• 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

THANK

YOU