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Somchodok Chakreeyarat, MD.

Endocrine Unit, Department of Medicine

Bhumibol Adulyadej Hospital


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Endocrine Unit, Department of MedicineBhumibol Adulyadej Hospital

Thyroid storm

Myxedema coma

Thyrotoxic periodic paralysis

Hyperglycemic crisis

Severe hypoglycemia

Hypercalcemia Hypocalcemia

Adrenal insufficiency


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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 thyrotoxicosisLow TSH, high FT4 or FT3

Etiology AD inherited defect in calcium or

sodium ion channel on musclemembrane

Thyrotoxicosis

Possible inherited predisposition

Penetrance Nonpenetrance common, esp inwoman

Epidemiology M > F M > F, high incidence in Asians

Preventive treatment

Carbonic anhydrase inhibitorsK+ sparing diuretics

Euthyroid statePropanolol


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ProminentU wave

ST depression


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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 PO4excretion

- 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


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K+

supplementation

Nonselective

beta blockers

Acute

Avoid precipitating

factors

Definite therapy

forhyperthyroidism

Chronic


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Nonselective beta blockers

Parenteral KCl might be given in saline instead of glucosesolution

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 incase of ventricular arrhythmia or impending respiratory failure


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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


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Life-threatening arrhythmia or

respiratory failure?

NO YES

Standart IV KCl infusion10mEq/hr

Rapid IV KCl infusion20-40 mEq/hr, then 10mEq/hr

Paradoxical hypokalemia

after KCl infusion

NO YES

Worsening hypokalemia and

life-threatening arrhythmiaYES

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


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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


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Most patients with TPP do not manifest typicalsymptoms 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


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Diabetic Ketoacidosis

(DKA)

Hyperglycemic

Hyperosmolar State(HHS)


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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 7.30

Serum bicarbonate (mEq/l) 15-18 10-15 15

Urine ketones* Positive Positive Positive Small

Serum ketones* Positive Positive Positive Small

Effective serum osmolality

(mOsm/kg)

Variable Variable Variable >320

Anion gap >10 >12 >12


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Beta-hydroxybutyrate,

the most important ketone

Beta-hydroxybutyrate,the most important

ketone


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Joint British Diabetes Society Inpatient (JBDS IP);2013recommend :

- Rapid near-patient technology 3-beta-hydroxybutyrate(BHB, HBA))


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DKA

To improve circulatory

volume and tissueperfusion

Decrease blood glucose

Correct the acidosisand electrolyte

imbalances

HHS

To gradually and safely

normalize theosmolarity

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


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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 standardurine sticks

Blood glucose > 200 mg/dL orknown DM

Venous or arterial HCO3 < 15mEq/L and/orpH < 7.3


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ADA 2009

Blood glucose < 200 mg/dl

Venous pH > 7.3

Serum bicarbonate 15

mEq/l

Calculated anion gap 12mEq/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)


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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 incrementshourly 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


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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 acidbase status


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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









* A slower infusion rate should be considered in young adults


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K+ Level in first 24 hr(mEq/L)

K+ Replacement in mEq/Lof infusion solution

> 5.5 Nil

3.5-5.5 40 mEq/L

< 3.5 Senior review


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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 : Criteria for diagnosis and Resolution


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ADA 2009

JBDS IP 2013

Startinsulin

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% glucoseif glucose < 200 mg/dL

Add 10% glucose ifglucose < 250 mg/dL

DKA : Insulin (RI or RAA) and IV fluid


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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


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Typical fluid and electrolyte losses in HHS (Kitabashi 2009)


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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

General rules


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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 180-270mg/dL in the first 24 hr

7. If blood glucose < 180 mg/dL commence 5% or 10%

dextrose at 125 mL/hr with NSS


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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.


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ADA 2009

JBDS IP 2013

Diagnosis Blood glucose >600mg/dL

Effective serum

osmolarity 320mosm/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 : Criteria for diagnosis and Resolution

HHS I li (RI RAA) d IV fl id


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ADA 2009 JBDS IP 2012

Startinsulin

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 adequatefluid resuscitation

Adjustinsulin

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% glucoseif glucose < 300 mg/dL

Add 5% or 10% glucoseif glucose < 180 mg/dL

HHS : Insulin (RI or RAA) and IV fluid


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Clotted

blood 10 ml

for :

1.Cortisol

2. Insulin

3. C-peptide

blood glucose < 50 mg/dL


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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/hrAdjust rate to normalize calcium

Start oral calcium and potent vitamin D

(eg, calcitriol or alfacalcidol)

Investigate the underlying cause (if not known) and treat


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Septic shock/severe sepsis

Replacement

therapy

3-18 g/dl > 18-20 g/dl

Morning cortisol 8 AM

Exclude

< 3 g/dl

ACTHstimulation test

Yes

No

Cortisol level


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Morning cortisol 8 AM

No

> 15 g/dl

Cortisol rise

> 34 g/dl

Adrenalfailure

Replacement

therapy

Cortisol rise> 9 g/dl

No adrenalfailure

No treatmentReplacement

therapy?

Cortisol rise

34 g/dl

Tissue resistanceto CS?

Cortisol rise 9 g/dl

< 15 g/dl

Adrenal failure

Replacementtherapy

Cortisol level

ACTH Stimulation test

Septic shock/severe sepsis

Yes


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Endocrine Unit, Department of MedicineBhumibol Adulyadej Hospital

Thyroid storm

Myxedema coma

Thyrotoxic periodic paralysis

Hyperglycemic crisis

Severe hypoglycemia

Hypercalcemia

Hypocalcemia

Adrenal insufficiency


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