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Somchodok Chakreeyarat, MD. 
Endocrine Unit, Department of Medicine 
Bhumibol Adulyadej Hospital
• Thyroid storm 
• Myxedema coma 
• Thyrotoxic periodic paralysis 
• Hyperglycemic crisis 
• Severe hypoglycemia 
• Hypercalcemia 
• Hypocalcemia 
Somchodok Chakreeyarat, MD. 
Endocrine Unit, Department of Medicine 
Bhumibol Adulyadej Hospital 
• Adrenal insufficiency
ACTEP2014: What's new in endocrine emergency
ACTEP2014: What's new in endocrine emergency
ACTEP2014: What's new in endocrine emergency
ACTEP2014: What's new in endocrine emergency
Hypokalemic periodic paralysis Thyrotoxic periodic paralysis 
Age at onset First or second decade > 20 years 
Attack frequency Infrequent Infrequent 
Attack duration Hours to days Hours to days 
Precipitants Exercise, CHO load, stress Exercise, CHO load, stress 
K+ level during attack Low Low 
Associated features Later onset myopathy Symptoms of thyrotoxicosis 
Low TSH, high FT4 or FT3 
Etiology AD inherited defect in calcium or 
sodium ion channel on muscle 
membrane 
Thyrotoxicosis 
Possible inherited predisposition 
Penetrance Nonpenetrance common, esp in 
woman 
Epidemiology M > F M > F, high incidence in Asians 
Preventive treatment Carbonic anhydrase inhibitors 
K+ sparing diuretics 
Euthyroid state 
Propanolol
ACTEP2014: What's new in endocrine emergency
ST depression 
Prominent 
U wave
Occurs in early morning or late evening 
Prodromal symptoms: muscle aches, cramps, muscle stiffness 
Begins in proximal muscle of the lower extremities 
 progress to flaccid quadriplegia 
Symmetrical, spared bulbar, respiratory and ocular muscle 
Serum K+ ↓, but not always during attack 
Spontaneous resolution within a few hours to 2 days 
“Thyrotoxic myopathy” persistent muscle weakness, soreness 
and normokalemia 
TPP can occur with any causes of hyperthyroidism
ECG finding 
- Sinus tachycardia or sinus arrhythmia 
- First degree AV block 
- LVH pattern 
Electrolytes and biochemistry in blood and urine 
- Hypo K+ with low urine excretion rate 
- Relatively normal blood acid-base balance 
- Hypo PO4 with low urine PO4 excretion 
- Normal or increased serum calcium with hypercalciuria 
- Hypocreatinemia ( increased GFR ) 
Therapeutic course 
- Lower K+ dose to achieve recovery 
- Rebound hyperkalemia if high K+ dose is given
K+ 
supplementation 
Nonselective 
beta blockers 
Acute 
Chronic 
Avoid precipitating 
factors 
Definite therapy 
for 
hyperthyroidism
Aim 
- To raise serum K+ rather than to fill a large K+ deficit 
- For the treatment of paralysis and prevention of fatal cardiac 
arrhythmia 
Close cardiac monitoring is absolutely warranted 
Exogenous KCl administration  rebound hyperkalemia 
Total KCl dose given less than 50 mEq, ↓ risk of rebound 
hyperkalemia 
KCl should be given at the rate of no more than 10 mEq/hr
Nonselective beta blockers 
Parenteral KCl might be given in saline instead of glucose 
solution 
Avoid oral route of KCl administration if bowel sounds are absent 
or diminished 
“ Hypokalemia-induced pseudointestinal obstruction” 
“Paradoxical hypokalemia” , a further fall in plasma K+ 
concentration during KCl therapy, associated with more severe 
hyperthyroidism and hyperadrenergic activity 
The maximum dose of KCl should be kept at 20-40 mEq/hr in 
case of ventricular arrhythmia or impending respiratory failure
Mechanism 
- To block K+ uptake via Na-K-ATPase 
Oral propanolol 3-4 mg/kg/day 
Shorten the duration of attack and promote recovery in TPP
Life-threatening arrhythmia or 
respiratory failure? 
NO YES 
Standart IV KCl infusion 
≤ 10 mEq/hr 
Rapid IV KCl infusion 
20-40 mEq/hr, then ≤ 10 mEq/hr 
Paradoxical hypokalemia 
after KCl infusion 
NO YES 
Worsening hypokalemia and 
life-threatening arrhythmia 
YES 
Keep the rate and stop KCl 
Infusion when muscle strength 
Increased 
Consider IV or oral non-selective 
beta blocker 
Recover from paralysis 
Chronic treatment for the 
underlying hyperthyroidism 
TPP 
NO
1. Avoid precipitating factors 
- High-carbohydrate diet 
- Exercise 
- Stress 
2. Definitive therapy for hyperthyroidism 
- Radioactive iodine ablation 
- Surgery 
- Antithyroid drugs 
3. Non-selective beta blockers 
- Preventing recurrent attacks of TPP
Most patients with TPP do not manifest typical 
symptoms and signs related to hyperthyroidism 
• Lab tests and ECG may help establish the diagnosis of TPP 
• In acute therapy, the dose of KCl should be minimal to 
rebound hyperkalemia, except in case of ventricular 
arrhythmia or impending respiratory insufficiency 
• High-dose non-selective beta blockers may be used to 
terminate muscle paralysis , esp for those who developed 
paradoxical hypokalemia
ACTEP2014: What's new in endocrine emergency
Diabetic Ketoacidosis 
(DKA) 
Hyperglycemic 
Hyperosmolar State 
(HHS)
DKA HHNS 
DKA 
Mild Moderate Severe HHNS 
Plasma glucose (mg/dl) >250 >250 >250 >600 
Arterial pH 7.25-7.30 7.00-7.24 <7.00 >7.30 
Serum bicarbonate (mEq/l) 15-18 10-15 <10 >15 
Urine ketones* Positive Positive Positive Small 
Serum ketones* Positive Positive Positive Small 
Effective serum osmolality 
Variable Variable Variable >320 
(mOsm/kg) 
Anion gap± >10 >12 >12 <12 
Alteration in sensorium 
or mental obtundation 
Alert Atert/drowsy Stupor/coma Stupor/coma 
*Nitroprusside reaction method; calculation: 2[measured Na (mEq/l)] + glucose (mg/dl)/18; 
±calculation (Na+) – (HCO3 
- + CI- ) (mEq/I).
ADA; 2009
ACTEP2014: What's new in endocrine emergency
ACTEP2014: What's new in endocrine emergency
ACTEP2014: What's new in endocrine emergency
Beta-hydroxybutyrate, 
the most important 
Beta-hydroxybutyrate, 
the most important ketone 
ketone
Joint British Diabetes Society Inpatient (JBDS IP);2013 
recommend : 
- Rapid near-patient technology  3-beta-hydroxybutyrate 
(BHB, ßHBA))
DKA 
• To improve circulatory 
volume and tissue 
perfusion 
• Decrease blood glucose 
• Correct the acidosis 
and electrolyte 
imbalances 
HHS 
• To gradually and safely 
normalize the 
osmolarity 
• Replace fluid and 
electrolyte loss 
• Normalize blood 
glucose 
Other goals include prevention of : 
• Arterial or venous thrombosis 
• Other potential complications e.g. 
cerebral oedema/ central pontine 
myelinolysis 
• Foot ulceration
ADA 2009 
• Blood glucose > 250 mg/dL 
• Ketonemia 
• Metabolic acidosis (pH ≤ 7.3) 
or serum HCO3 < 18 mEq/L 
JBDS IP 2013 
• BHB > 3 mmol/L or Urine 
ketone ≥ 2+ on standard 
urine sticks 
• Blood glucose > 200 mg/dL or 
known DM 
• Venous or arterial HCO3 < 15 
mEq/L and/or pH < 7.3
ADA 2009 
• Blood glucose < 200 mg/dl 
• Venous pH > 7.3 
• Serum bicarbonate ≥ 15 
mEq/l 
• Calculated anion gap ≤12 
mEq/l 
JBDS IP 2013 
• Venous pH > 7.3 
• Bicarbonate > 15.0 mEq/L 
• BHB level < 0.6 mmol/L 
(rather than < 0.3 mmol/L)
1. Bedsides ketone (BHB) testing now represents the best 
practice in monitoring the response to treatment 
2. Fixed Rate Insulin Infusion (FRII) with short acting or 
rapid acting insulin 0.1 unit/kg/hr should be used with 
an infusion pump 
3. Do not use a priming (bolus) dose of insulin
4. Adjusted insulin dose if the metabolic target are not met 
- Reduction of blood ketone(BHB) at least 0.5 
mmol/L/hour 
- Increase in venous HCO3 at least 3 mEq/L/hour 
- Reduction in CBG at least 50 mg/dL/hour 
5. Increase insulin infusion rate by 1.0 unit/hr increments 
hourly until the ketones are falling at target rates 
6. Measure venous blood gas for pH,HCO3, and K+ at 60 
min, and then q 2 hr
The difference between venous and arterial pH is 
0.02- 0.15 pH units 
The difference between arterial and venous bicarbonate 
is 1.88 mmol/L 
It is not necessary to use arterial blood to measure acid 
base status
Fluid Volume 
1 L 0.9% NaCl 1,000 mL over first hour 
1 L 0.9% NaCl with KCl 1,000 mL over next 2 hr 
1 L 0.9% NaCl with KCl 1,000 mL over next 2 hr 
1 L 0.9% NaCl with KCl 1,000 mL over next 4 hr 
1 L 0.9% NaCl with KCl 1,000 mL over next 4 hr 
1 L 0.9% NaCl with KCl 1,000 mL over next 6 hr 
* A slower infusion rate should be considered in young adults
K+ Level in first 24 hr 
(mEq/L) 
K+ Replacement in mEq/L 
of infusion solution 
> 5.5 Nil 
3.5-5.5 40 mEq/L 
< 3.5 Senior review
DKA : Criteria for diagnosis and Resolution 
ADA 2009 JBDS IP 2013 
Diagnosis • Blood glucose > 250 mg/dL 
• Ketonemia 
• Metabolic acidosis(pH ≤ 7.3) 
or serum HCO3 < 18 mEq/L 
• BHB > 3 mmol/L or 
Urine ketone ≥ 2+ on 
standard urine sticks 
• Blood glucose > 200 mg/dL 
or known DM 
• Venous or arterial HCO3 
< 15 mEq/L and/or 
pH < 7.3 
Resolution • Venous pH > 7.3 
• Serum bicarbonate ≥ 15 
mEq/l 
• Blood glucose < 200 mg/dl 
• Calculated anion gap ≤12 
mEq/l 
• Venous pH > 7.3 
• Bicarbonate > 15 mEq/L 
• BHB level < 0.6 mmol/L 
(rather than < 0.3 mmol/L)
DKA : Insulin (RI or RAA) and IV fluid 
ADA 2009 JBDS IP 2013 
Start 
insulin 
• 0.1 unit/kg IV bolus 
• 0.1 unit/kg/hr CII 
• No bolus 
• 0.1 unit/kg/hr CII 
Adjust 
insulin 
Bolus 0.14 unit/kg if 
• serum glucose < 10%/hr 
Increase insulin infusion 
rate by 1.0 unit/hr If 
• BHB  < 0.5 mmol/L/hr 
• Venous HCO3  < 3 
mEq/L/hour 
• CBG  < 50 mg/dL/hour 
IV fluid • Change IV to 5% glucose 
if glucose < 200 mg/dL 
• Add 10% glucose if 
glucose < 250 mg/dL
ACTEP2014: What's new in endocrine emergency
Characteristic features of a person with HHS: 
• High osmolality, often 320 mosmol/kg or more 
• High blood glucose, usually 30 mmol/L 
• • 
(540 mg/dL) or more 
• Severely dehydrated and unwell
Typical fluid and electrolyte losses in HHS (Kitabashi 2009)
General rules 
1. The goal of initial therapy is to expand the intra- and 
extravascular volume and to restore peripheral 
perfusion 
2. An optimal rate of decline in serum sodium of 0.5 
mEq/L/hr has been recommended for hypernatremic 
dehydration and not fall exceed 10-12 mEq/L/day 
3. If BHB > 1 mmol/L = hypoinsuilinemia  start insulin 
If BHB is not present insulin should not be started
Is 
4. Insulin treatment prior to adequate fluid 
replacement may result in cardiovascular collapse 
5. The recommended insulin dose is an FRII given at 
0.05 units/kg/hr . A fall of glucose at a rate of up to 
90 mg/dL/hr is ideal 
6. Avoid hypoglycemia. Target blood glucose is 180-270 
mg/dL in the first 24 hr 
7. If blood glucose < 180 mg/dL commence 5% or 10% 
dextrose at 125 mL/hr with NSS
The target: 
The aim of treatment should be to replace 
approximately 50% of estimated fluid loss within the 
first 12 Hours 
The remainder in the following 12 hours 
A target blood glucose of between 180 and 270 mg/dL 
Complete normalisation of electrolytes and osmolality 
may take up to 72 hours.
HHS : Criteria for diagnosis and Resolution 
ADA 2009 JBDS IP 2013 
Diagnosis • Blood glucose >600 
mg/dL 
• Effective serum 
osmolarity ≥320 
mosm/kg 
• High osmolality, often 
320 mosm/kg or more 
• High blood glucose, 
usually 30 mmol/L 
(540 mg/dL) or more 
• Severely dehydrated 
and unwell 
Resolution • Normal osmolality 
• Regain of normal 
mental status 
• Normal osmolality 
• Regain of normal 
mental status
HHS : Insulin (RI or RAA) and IV fluid 
ADA 2009 JBDS IP 2012 
Start 
insulin 
• 0.1 unit/kg IV bolus 
• 0.1 unit/kg/hr CII 
• No bolus 
• 0.05 unit/kg/hr CII if 
BHB > 1 mmo/L or 
serum glucose < 90 
mg/dL after adequate 
fluid resuscitation 
Adjust 
insulin 
Bolus 0.14 unit/kg if 
• serum glucose < 10%/hr 
• Increase insulin 
infusion rate by 1.0 
unit/hr if not achieve 
target 
IV fluid • Change IV to 5% glucose 
if glucose < 300 mg/dL 
• Add 5% or 10% glucose 
if glucose < 180 mg/dL
แนวทางการสืบค้นสาหรับผู้ป่วยที่มีระดับน้าตาลในเลือดต่า 
Clotted 
blood 10 ml 
for : 
1.Cortisol 
2. Insulin 
3. C-peptide 
blood glucose < 50 mg/dL
Tetany, seizures, laryngospasm, or cardiac dysfunction 
with proven or strong suspicion of low calcium 
10-20 mL of 10% calcium gluconate in 50-100 mL 5% dextrose 
(or 0.9% saline) given over 10 min with EKG monitoring 
Repeat above treatment until symptom-free 
• Treat hypomagnesemia (if present) with IV magnesium 
sulfate 
Start IV infusion of 100 mL of 10% calcium gluconate in 1 L of 
normal (0.9%) saline (or 5% dextrose) at a rate of 50-100 mL/hr 
Adjust rate to normalize calcium 
Start oral calcium and potent vitamin D 
(eg, calcitriol or alfacalcidol) 
• Investigate the underlying cause (if not known) and treat
ACTEP2014: What's new in endocrine emergency
Cushing’s 
syndrome
Septic shock/severe sepsis 
Replacement 
therapy 
No Yes 
Morning cortisol 8 AM 
3-18 μg/dl > 18-20 μg/dl 
Exclude 
< 3 μg/dl 
ACTH 
stimulation test 
Cortisol level
No 
Septic shock/severe sepsis 
Morning cortisol 8 AM 
> 15 μg/dl 
Cortisol rise 
> 34 μg/dl 
Adrenal 
failure 
Replacement 
therapy 
Cortisol rise 
> 9 μg/dl 
No adrenal 
failure 
Cortisol rise 
≤ 34 μg/dl 
Tissue resistance 
to CS? 
No treatment Replacement 
therapy? 
Cortisol rise 
≤ 9 μg/dl 
< 15 μg/dl 
Adrenal failure 
Replacement 
therapy 
Cortisol level 
ACTH Stimulation test 
Yes
• Thyroid storm 
• Myxedema coma 
• Thyrotoxic periodic paralysis 
• Hyperglycemic crisis 
• Severe hypoglycemia 
• Hypercalcemia 
• Hypocalcemia 
Somchodok Chakreeyarat, MD. 
Endocrine Unit, Department of Medicine 
Bhumibol Adulyadej Hospital 
• Adrenal insufficiency
ACTEP2014: What's new in endocrine emergency

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ACTEP2014: What's new in endocrine emergency

  • 1. Somchodok Chakreeyarat, MD. Endocrine Unit, Department of Medicine Bhumibol Adulyadej Hospital
  • 2. • Thyroid storm • Myxedema coma • Thyrotoxic periodic paralysis • Hyperglycemic crisis • Severe hypoglycemia • Hypercalcemia • Hypocalcemia Somchodok Chakreeyarat, MD. Endocrine Unit, Department of Medicine Bhumibol Adulyadej Hospital • Adrenal insufficiency
  • 7. Hypokalemic periodic paralysis Thyrotoxic periodic paralysis Age at onset First or second decade > 20 years Attack frequency Infrequent Infrequent Attack duration Hours to days Hours to days Precipitants Exercise, CHO load, stress Exercise, CHO load, stress K+ level during attack Low Low Associated features Later onset myopathy Symptoms of thyrotoxicosis Low TSH, high FT4 or FT3 Etiology AD inherited defect in calcium or sodium ion channel on muscle membrane Thyrotoxicosis Possible inherited predisposition Penetrance Nonpenetrance common, esp in woman Epidemiology M > F M > F, high incidence in Asians Preventive treatment Carbonic anhydrase inhibitors K+ sparing diuretics Euthyroid state Propanolol
  • 10. Occurs in early morning or late evening Prodromal symptoms: muscle aches, cramps, muscle stiffness Begins in proximal muscle of the lower extremities  progress to flaccid quadriplegia Symmetrical, spared bulbar, respiratory and ocular muscle Serum K+ ↓, but not always during attack Spontaneous resolution within a few hours to 2 days “Thyrotoxic myopathy” persistent muscle weakness, soreness and normokalemia TPP can occur with any causes of hyperthyroidism
  • 11. ECG finding - Sinus tachycardia or sinus arrhythmia - First degree AV block - LVH pattern Electrolytes and biochemistry in blood and urine - Hypo K+ with low urine excretion rate - Relatively normal blood acid-base balance - Hypo PO4 with low urine PO4 excretion - Normal or increased serum calcium with hypercalciuria - Hypocreatinemia ( increased GFR ) Therapeutic course - Lower K+ dose to achieve recovery - Rebound hyperkalemia if high K+ dose is given
  • 12. K+ supplementation Nonselective beta blockers Acute Chronic Avoid precipitating factors Definite therapy for hyperthyroidism
  • 13. Aim - To raise serum K+ rather than to fill a large K+ deficit - For the treatment of paralysis and prevention of fatal cardiac arrhythmia Close cardiac monitoring is absolutely warranted Exogenous KCl administration  rebound hyperkalemia Total KCl dose given less than 50 mEq, ↓ risk of rebound hyperkalemia KCl should be given at the rate of no more than 10 mEq/hr
  • 14. Nonselective beta blockers Parenteral KCl might be given in saline instead of glucose solution Avoid oral route of KCl administration if bowel sounds are absent or diminished “ Hypokalemia-induced pseudointestinal obstruction” “Paradoxical hypokalemia” , a further fall in plasma K+ concentration during KCl therapy, associated with more severe hyperthyroidism and hyperadrenergic activity The maximum dose of KCl should be kept at 20-40 mEq/hr in case of ventricular arrhythmia or impending respiratory failure
  • 15. Mechanism - To block K+ uptake via Na-K-ATPase Oral propanolol 3-4 mg/kg/day Shorten the duration of attack and promote recovery in TPP
  • 16. Life-threatening arrhythmia or respiratory failure? NO YES Standart IV KCl infusion ≤ 10 mEq/hr Rapid IV KCl infusion 20-40 mEq/hr, then ≤ 10 mEq/hr Paradoxical hypokalemia after KCl infusion NO YES Worsening hypokalemia and life-threatening arrhythmia YES Keep the rate and stop KCl Infusion when muscle strength Increased Consider IV or oral non-selective beta blocker Recover from paralysis Chronic treatment for the underlying hyperthyroidism TPP NO
  • 17. 1. Avoid precipitating factors - High-carbohydrate diet - Exercise - Stress 2. Definitive therapy for hyperthyroidism - Radioactive iodine ablation - Surgery - Antithyroid drugs 3. Non-selective beta blockers - Preventing recurrent attacks of TPP
  • 18. Most patients with TPP do not manifest typical symptoms and signs related to hyperthyroidism • Lab tests and ECG may help establish the diagnosis of TPP • In acute therapy, the dose of KCl should be minimal to rebound hyperkalemia, except in case of ventricular arrhythmia or impending respiratory insufficiency • High-dose non-selective beta blockers may be used to terminate muscle paralysis , esp for those who developed paradoxical hypokalemia
  • 20. Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS)
  • 21. DKA HHNS DKA Mild Moderate Severe HHNS Plasma glucose (mg/dl) >250 >250 >250 >600 Arterial pH 7.25-7.30 7.00-7.24 <7.00 >7.30 Serum bicarbonate (mEq/l) 15-18 10-15 <10 >15 Urine ketones* Positive Positive Positive Small Serum ketones* Positive Positive Positive Small Effective serum osmolality Variable Variable Variable >320 (mOsm/kg) Anion gap± >10 >12 >12 <12 Alteration in sensorium or mental obtundation Alert Atert/drowsy Stupor/coma Stupor/coma *Nitroprusside reaction method; calculation: 2[measured Na (mEq/l)] + glucose (mg/dl)/18; ±calculation (Na+) – (HCO3 - + CI- ) (mEq/I).
  • 26. Beta-hydroxybutyrate, the most important Beta-hydroxybutyrate, the most important ketone ketone
  • 27. Joint British Diabetes Society Inpatient (JBDS IP);2013 recommend : - Rapid near-patient technology  3-beta-hydroxybutyrate (BHB, ßHBA))
  • 28. DKA • To improve circulatory volume and tissue perfusion • Decrease blood glucose • Correct the acidosis and electrolyte imbalances HHS • To gradually and safely normalize the osmolarity • Replace fluid and electrolyte loss • Normalize blood glucose Other goals include prevention of : • Arterial or venous thrombosis • Other potential complications e.g. cerebral oedema/ central pontine myelinolysis • Foot ulceration
  • 29. ADA 2009 • Blood glucose > 250 mg/dL • Ketonemia • Metabolic acidosis (pH ≤ 7.3) or serum HCO3 < 18 mEq/L JBDS IP 2013 • BHB > 3 mmol/L or Urine ketone ≥ 2+ on standard urine sticks • Blood glucose > 200 mg/dL or known DM • Venous or arterial HCO3 < 15 mEq/L and/or pH < 7.3
  • 30. ADA 2009 • Blood glucose < 200 mg/dl • Venous pH > 7.3 • Serum bicarbonate ≥ 15 mEq/l • Calculated anion gap ≤12 mEq/l JBDS IP 2013 • Venous pH > 7.3 • Bicarbonate > 15.0 mEq/L • BHB level < 0.6 mmol/L (rather than < 0.3 mmol/L)
  • 31. 1. Bedsides ketone (BHB) testing now represents the best practice in monitoring the response to treatment 2. Fixed Rate Insulin Infusion (FRII) with short acting or rapid acting insulin 0.1 unit/kg/hr should be used with an infusion pump 3. Do not use a priming (bolus) dose of insulin
  • 32. 4. Adjusted insulin dose if the metabolic target are not met - Reduction of blood ketone(BHB) at least 0.5 mmol/L/hour - Increase in venous HCO3 at least 3 mEq/L/hour - Reduction in CBG at least 50 mg/dL/hour 5. Increase insulin infusion rate by 1.0 unit/hr increments hourly until the ketones are falling at target rates 6. Measure venous blood gas for pH,HCO3, and K+ at 60 min, and then q 2 hr
  • 33. The difference between venous and arterial pH is 0.02- 0.15 pH units The difference between arterial and venous bicarbonate is 1.88 mmol/L It is not necessary to use arterial blood to measure acid base status
  • 34. Fluid Volume 1 L 0.9% NaCl 1,000 mL over first hour 1 L 0.9% NaCl with KCl 1,000 mL over next 2 hr 1 L 0.9% NaCl with KCl 1,000 mL over next 2 hr 1 L 0.9% NaCl with KCl 1,000 mL over next 4 hr 1 L 0.9% NaCl with KCl 1,000 mL over next 4 hr 1 L 0.9% NaCl with KCl 1,000 mL over next 6 hr * A slower infusion rate should be considered in young adults
  • 35. K+ Level in first 24 hr (mEq/L) K+ Replacement in mEq/L of infusion solution > 5.5 Nil 3.5-5.5 40 mEq/L < 3.5 Senior review
  • 36. DKA : Criteria for diagnosis and Resolution ADA 2009 JBDS IP 2013 Diagnosis • Blood glucose > 250 mg/dL • Ketonemia • Metabolic acidosis(pH ≤ 7.3) or serum HCO3 < 18 mEq/L • BHB > 3 mmol/L or Urine ketone ≥ 2+ on standard urine sticks • Blood glucose > 200 mg/dL or known DM • Venous or arterial HCO3 < 15 mEq/L and/or pH < 7.3 Resolution • Venous pH > 7.3 • Serum bicarbonate ≥ 15 mEq/l • Blood glucose < 200 mg/dl • Calculated anion gap ≤12 mEq/l • Venous pH > 7.3 • Bicarbonate > 15 mEq/L • BHB level < 0.6 mmol/L (rather than < 0.3 mmol/L)
  • 37. DKA : Insulin (RI or RAA) and IV fluid ADA 2009 JBDS IP 2013 Start insulin • 0.1 unit/kg IV bolus • 0.1 unit/kg/hr CII • No bolus • 0.1 unit/kg/hr CII Adjust insulin Bolus 0.14 unit/kg if • serum glucose < 10%/hr Increase insulin infusion rate by 1.0 unit/hr If • BHB  < 0.5 mmol/L/hr • Venous HCO3  < 3 mEq/L/hour • CBG  < 50 mg/dL/hour IV fluid • Change IV to 5% glucose if glucose < 200 mg/dL • Add 10% glucose if glucose < 250 mg/dL
  • 39. Characteristic features of a person with HHS: • High osmolality, often 320 mosmol/kg or more • High blood glucose, usually 30 mmol/L • • (540 mg/dL) or more • Severely dehydrated and unwell
  • 40. Typical fluid and electrolyte losses in HHS (Kitabashi 2009)
  • 41. General rules 1. The goal of initial therapy is to expand the intra- and extravascular volume and to restore peripheral perfusion 2. An optimal rate of decline in serum sodium of 0.5 mEq/L/hr has been recommended for hypernatremic dehydration and not fall exceed 10-12 mEq/L/day 3. If BHB > 1 mmol/L = hypoinsuilinemia  start insulin If BHB is not present insulin should not be started
  • 42. Is 4. Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse 5. The recommended insulin dose is an FRII given at 0.05 units/kg/hr . A fall of glucose at a rate of up to 90 mg/dL/hr is ideal 6. Avoid hypoglycemia. Target blood glucose is 180-270 mg/dL in the first 24 hr 7. If blood glucose < 180 mg/dL commence 5% or 10% dextrose at 125 mL/hr with NSS
  • 43. The target: The aim of treatment should be to replace approximately 50% of estimated fluid loss within the first 12 Hours The remainder in the following 12 hours A target blood glucose of between 180 and 270 mg/dL Complete normalisation of electrolytes and osmolality may take up to 72 hours.
  • 44. HHS : Criteria for diagnosis and Resolution ADA 2009 JBDS IP 2013 Diagnosis • Blood glucose >600 mg/dL • Effective serum osmolarity ≥320 mosm/kg • High osmolality, often 320 mosm/kg or more • High blood glucose, usually 30 mmol/L (540 mg/dL) or more • Severely dehydrated and unwell Resolution • Normal osmolality • Regain of normal mental status • Normal osmolality • Regain of normal mental status
  • 45. HHS : Insulin (RI or RAA) and IV fluid ADA 2009 JBDS IP 2012 Start insulin • 0.1 unit/kg IV bolus • 0.1 unit/kg/hr CII • No bolus • 0.05 unit/kg/hr CII if BHB > 1 mmo/L or serum glucose < 90 mg/dL after adequate fluid resuscitation Adjust insulin Bolus 0.14 unit/kg if • serum glucose < 10%/hr • Increase insulin infusion rate by 1.0 unit/hr if not achieve target IV fluid • Change IV to 5% glucose if glucose < 300 mg/dL • Add 5% or 10% glucose if glucose < 180 mg/dL
  • 47. Tetany, seizures, laryngospasm, or cardiac dysfunction with proven or strong suspicion of low calcium 10-20 mL of 10% calcium gluconate in 50-100 mL 5% dextrose (or 0.9% saline) given over 10 min with EKG monitoring Repeat above treatment until symptom-free • Treat hypomagnesemia (if present) with IV magnesium sulfate Start IV infusion of 100 mL of 10% calcium gluconate in 1 L of normal (0.9%) saline (or 5% dextrose) at a rate of 50-100 mL/hr Adjust rate to normalize calcium Start oral calcium and potent vitamin D (eg, calcitriol or alfacalcidol) • Investigate the underlying cause (if not known) and treat
  • 50. Septic shock/severe sepsis Replacement therapy No Yes Morning cortisol 8 AM 3-18 μg/dl > 18-20 μg/dl Exclude < 3 μg/dl ACTH stimulation test Cortisol level
  • 51. No Septic shock/severe sepsis Morning cortisol 8 AM > 15 μg/dl Cortisol rise > 34 μg/dl Adrenal failure Replacement therapy Cortisol rise > 9 μg/dl No adrenal failure Cortisol rise ≤ 34 μg/dl Tissue resistance to CS? No treatment Replacement therapy? Cortisol rise ≤ 9 μg/dl < 15 μg/dl Adrenal failure Replacement therapy Cortisol level ACTH Stimulation test Yes
  • 52. • Thyroid storm • Myxedema coma • Thyrotoxic periodic paralysis • Hyperglycemic crisis • Severe hypoglycemia • Hypercalcemia • Hypocalcemia Somchodok Chakreeyarat, MD. Endocrine Unit, Department of Medicine Bhumibol Adulyadej Hospital • Adrenal insufficiency