1

Emergency in endocrine

system
Acute Complication of Diabetes

Dr.MMD
 3

Serious acute complications of diabetes

Diabetic ketoacidosis (DKA)

Hyperosmolar hyperglycemic state (HHS)
Hypoglycemia
 4

DKA

Diabetic Ketoacidosis

Most serious complication in Type 1 diabetes

 5

Diabetic Ketoacidosis (DKA)

Elevated blood glucose levels (250 mg/dL
but usually <600 mg/dL)
Presence of ketones in blood and urine
Polyuria, polydipsia, hyperventilation,
dehydration, fruity odor, fatigue
Can lead to coma and death
Often occurs during acute illness (flu, colds,
vomiting and diarrhea)
 6

Precipitating Causes

Not enough insulin

Skipping insulin
Stress, trauma
Insulin resistance
 7

Pathophysiology of DKA

Ketosis
Dehydration
Electrolyte imbalance
 8

DIABETES CARE, VOLUME 29, NUMBER 12, DECEMBER 2006

 10

Symptoms of DKA
Abdominal pain Polyuria
Anorexia Somnolence
Dehydration Tachycardia
Fuity breath Thirst
Kussmauls Visual disturbances
Change LOC Warm, dry skin
Hypotension Weakness
Wt. loss
 11

Assessment DKA
Hyperglycemia
Hyperosmolality
Dehydration
Electrolyte imbalances
Metabolic acidosis
Hypoglycemia
Fluid overload
12
 13

Intervention

Rehydrate
Reverse shock
Give Potassium
Corret pH
Give insulin
 14

Critical Monitoring

Rehydration
Daily Weight
Skin turgor, LOC, VS
CVP measurement
Auscultation of lungs
 15

IV Fluids in DKA

Hour 1
N/S or Ringers lactate (15-20ml/kg)
Hour 2
Continue fluid, consider half-strength NS
Hour 3
Reduce fluid intake to 7.5ml/kg, use half-strength NS
Hour 4
Consider urine output in adjusting fluids
 16

To calculate the actual fluid deficit by the use of formula:

POsm (patient) POsm (normal)
Fluid deficit (liters) = x body waters (liters)
POsm (normal)
POsm (normal) = 290 295 mOsm/liter;
Body water is calculated as ideal body weight (kg) x 0,65

After the initial 2 hour the remainder of the fluid deficit is given at
the rate of 1 liter/hour.
 17

Potassium Replacement in DKA

Look at EKG
Replacement is based on plasma potassium
level
Recheck potassium q 2 hours
 18

Correct pH/Give Insulin

Give IV Insulin
Give Regular Insulin only
Initial bolus IV (0.15u/kg)
Then Regular Insulin IV drip
 19

HHNK
Hyperglycemic Hyperosmolar Noketotic Syndrome

Most commonly occurs in older adults with

Type 2 diabetes
Always look for precipitating factors
 20

Hyperosmolar Hyperglycemic
State
Extremely high blood glucose level (600-
2000 mg/dL)
Absence of or small amounts of ketones
Profound dehydration
Pts have sufficient insulin to prevent lipolysis
and ketosis
Occurs in older patients with type 2 diabetes
Treatment: hydration and small doses of
insulin to correct the hyperglycemia
 21

Plasma osmolality is calculated by the equation:

Glucose BUN
2(Na + K) + + mOsm/liter
18 2,8

Na and K are in mEq/l; glucose in mg/dl; BUN in mg/dl

 22

Treatment

Similar to DKA
Find underlying cause
23
 24

Hypoglycemia

Also known as insulin reaction or

hypoglycemic reaction
 Hypoglycemia is an abnormally low plasma
glucose level that leads to symptoms of
sympathetic NS stimulation or of CNS
dysfunction.

The Merck Manual of Diagnosis and Therapy

Seventeenth Edition (1999)
 Blood Glucose
Normal Blood Glucosa 60-100 mg/dL

Hypoglycemia: BG <50 mg/dL in men;

<45 mg/dL in women
 Requirements for Diagnosis
Whipples Triad
Symptoms of hypoglycemia
Blood glucose levels <50 mg/dL in men or <45
mg/dL in women
Alleviation of symptoms after correction of the
low BG levels (ingestion of sugar)
 28

Risk Factors

Overdose of insulin
Omitting a meal
Overexertion
Nausea and vomiting
Alcohol intake
 PHYSIOLOGY OF
GLUCOSE COUNTERREGULATION
Characteristic sequence:

1. insulin secretion:
glucose concentrations decline within the physiological range (72
108 mg/dl /4.06.0 mmol/l).

2. glucagon and epinephrine secretion:

glucose concentrations fall just below the physiological range
(6570 mg/dl (3.63.9 mmol/l).

3. Neurogenic and neuroglycopenic symptoms and cognitive

impairments: in range (5055 mg/dl (2.8 3.0 mmol/l).
 Liver glucose output responds to multiple hormonal signals

Antonio Vidal -Puig & Stephen O'rahilly (2001) Nature 413, 125 126.
 31

Symptoms of Hypoglycemia
Adrenergic Neuroglycopenic
Shakiness Headache
Irritability Mental illness
Nervousness Inability to
Tachycardia concentrate
Tremor Slurred speech
Hunger Blurred vision
Diaphoresis Confusion
Pallor Irrational behavior
Paresthesias Lethargy
LOC, coma,
 34

Interventions

Mild
carbohydrate 10-15 gram
Moderate
20-30 gram of carbs
Glucagon, 1 mg SC or IM
Severe
50% dextrose 25 g IV
Glucagon 1 mg IM or IV
HYPOGLYCEMIA IN DIABETES
CLINICAL RISK FACTORS FOR HYPOGLYCEMIA
IN DIABETES

Absolute or relative insulin excess occurs when

1. doses Insulin (or insulin secretagogue or sensitizer)

2. Exogenous glucose delivery.
3. Endogenous glucose production
4. Glucose utilization
5. Sensitivity to insulin
6. Insulin clearance
Sulfonylureas : hypoglycemic risk

RR

Tolbutamide 1
Gliclazide 1 - 2(2)
Repaglinide 1-2
Glipizide 2(1)
Glimepiride 3 - 4(3)
Glibenclamide 5(1)

1) Ferner 1988
(2) Teisse, Diab Med,1994
(3) Dills, Horm Metab Res,1996
 Hypoglycemic risk

Glibenclamide has greatest risk for hypoglycemia (less so when

given 2-3 times a day in smaller portions)

Repaglinide (3 times a day) seems to have smallest risk, but needs

more confirmation on its efficacy in severe DM.

Although different receptor-binding explains this difference, the

small doses used is crucial.
HYPOGLYCEMIA-ASSOCIATED AUTONOMIC FAILURE

(1) counterregulatory hormone responses (type 1 diabetes)

- insulin levels do not decline as glucose levels fall (first
defense lost)
- glucagon response diminishes (the second defense lost)
- epinephrine response reduced (third defense lost)

(2) hypoglycemia unawareness.

a loss of the warning symptoms
the first manifestation of hypoglycemia
 Somogyi Effect
Rebound hyperglycemia
Counterregulatory hormones activate
gluconeogenesis and glycogenolysis
Hormones supress insulin 12-48 hours
Also influenced by excessive carb intake
Somogyi Effect
 Thyroid Storm
A life-threatening crisis .
Estimated mortality : 20-30% .
the result of thyroid surgery .
Caused more often by antecedent Graves
disease .
 Precipitants of Thyroid Storm
Surgery .
Radioiodine therapy .
Iodinated contrast dyes .
Thyroid hormone ingestion .
Diabetic Ketoacidosis .
Cerebrovascular accident .
Pulmonary embolism and CHF .
 Pathophysiology of Thyroid
Storm
1) An acute decrease in thyroxine-binding
globulin => high levels of free hormone .
2) Thyroid hormone increases the density of
beta-adrenergic receptors & alters
responsiveness to catecholamines at a
postreceptor level .
Laboratory Diagnosis of Thyroid
Storm
A combination of low TSH and elevated
free T4 => makes the diagnosis .
If TSH is lower than normal and free T4 is
normal => free T3 testing is recommended .
ED measurement of thyroglobulin or thyroid
antibodies : No indication .
 Treatment of Thyroid Storm
Block hormone synthesis with either :
a) Propylthiouracil 100-600 mg loading PO
or NG , 200-250 mg q4h for total daily dose
of 1200-1500 mg ; or
b) methimazole 20 mg PO ( 10-40 mg
range ) q 4h .
 Treatment of Thyroid Storm (
continued )
Inhibit hormone release :
Iodides Potassium iodide ( SSKI ) 5 drops PO
Q6-8H , or
Lugols solution 7-8 drops ( 1 mL PO Q6H ) or
Ipodate 1-3 g daily ( as 1 g Q8H for 24 hours ,
then 500 mg Q12H ) .
If severe iodide allergy , lithium carbonate 300 mg
Q6H .
 Treatment of Thyroid Storm (
continued )
Glucocorticoids : Hydrocortisone ( 300 mg
IV , then 100 mg IV q8h ) ; dexamethasone
( 2 mg Q6H ) .
Adrenergic blockade : Propranolol ( 0.5-3
mg IV over 15 minutes slow IV , then 60-80
mg PO Q4H ) ; Esmolol ( 0.25-0.5 mcg/kg
loading , infusion of 0.05-0.1 mcg/kg/min )
.
 Adjunctive Therapy for Thyroid
Storm
Treat fever aggressively with
acetaminophen .
IV fluid containing 10% dextrose are
recommended .
Administer vitamin supplements , including
thiamine .
Treat CHF with conventional methods .
 Adjunctive Therapy for Thyroid
Storm ( continued )
Identify the precipitating event , including
infection .
Consider plasmapheresis , hemodialysis or
peritoneal dialysis for removal of
metabolically active hormone .
 Thyrotoxic Periodic Paralysis

Most common cause of hypokalemic periodic

paralysis
Flaccid paralysis
Lower extremities affected most often
Ocular and bulbar muscles uninvolved,
respiratory muscles rarely involved
Most often starts during sleep
Precipitated following exercise, high
salt intake or high carbohydrate diet
Hypokalemia during the paralysis