سيمنارات

Endocrinological Emergencies

Mosul Medical College
Department of Medicine

Presented by:

Dr. Salam Fareed
8/21/2016

Diabetic ketoacidosis

8/21/2016
INTRODUCTION
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes-20%.
This condition is a complex disordered metabolic
state characterized by:
hyperglycemia: blood glucose level > 200 mg/ dl
Ketoacidosis: ketonuria > ++ on standard urine sample.
Metabolic acidosis: PH < 7.3, s. bicarbonate < 15


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Pathophysiology
DKA typically occurs in the setting of hyperglycemia with relative or absolute insulin deficiency and an increase in counterregulatory hormones.
Sufficient amounts of insulin are not present to suppress lipolysis and oxidation of free fatty acids, which results in ketone body production and subsequent metabolic acidosis.
DKA occurs more frequently with type 1 diabetes, although 10% to 30% of cases occur in patients with type 2 diabetes.

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Predisposing Factors
Several risk factors can precipitate the development of extreme hyperglycemia:
infection(UTI).
intentional or inadvertent insulin therapy omission.
myocardial infarction.
Stress.
trauma.
confounding medications, such as glucocorticoids or atypical antipsychotic agents.

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Clinical Presentation
The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA:
-may be the 1st presentation
Malaise, generalized weakness, and fatigability
Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia
Rapid weight loss in patients newly diagnosed with type 1 diabetes
History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump
Decreased perspiration
Altered consciousness (eg, mild disorientation, confusion)


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Signs and symptoms of DKA associated with possible intercurrent infection are as follows:

Fever

Coughing
Chills
Chest pain
Dyspnea
Arthralgia
Urinary symptoms
Hormones affect insulin level CortisoneNor adrenaline Gulcagon

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On examination
Ill appearance
Dry skin
Labored respiration
Dry mucous membranes
Decreased skin turgor
Decreased reflexes
Characteristic acetone (ketotic) breath odor
Tachycardia
Hypotension
Tachypnea


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Investigations:

Serum glucose levels

Serum electrolyte levels
Amylase and lipase levels
Urine dipstick
Ketone levels
ABG measurements
CBC count
BUN and creatinine levels
C-RP
Urine and blood cultures if intercurrent infection is suspected
ECG(hyper-k+=peaked T wave+no ST segment+widening of QRS)
Chest radiography: to rule out pulmonary infection
Head CT scanning: to detect early cerebral edema.

normal urea ( < 40 mg/dl)Normal creatinine( <1.2 mg/dl)

hyper-k+=
peaked T wave+no ST segment+widening of QRS

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Management:
Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable.
Plan for therapy:
When treating patients with DKA, the following points must be considered and closely monitored:
Correction of fluid loss with intravenous fluids
Correction of hyperglycemia with insulin
Correction of electrolyte disturbances, particularly potassium loss
Correction of acid-base balance
Treatment of concurrent infection, if present
ب DKA ما تنزل السكري بسرعةﻻن اذا نزل بسرعة يعمل Cerebral odema

8/21/2016

Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows:


Blood tests for glucose every 1-2 h until patient is stable, then every 4-6 h
Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h
Initial blood urea
Initial arterial blood gas (ABG) measurements, followed with bicarbonate as necessary

Example how to arrange a chart to follow a DKA patient

S. k
RBS
Output
Input fluid
Insulin
BP
Time
6.2
410
Nil
2 L/NS
20 units IM
80/50
3:00 PM


4:00 PM
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S. k

RBS
Output
Input fluid
Insulin
BP
Time
6.2
620
Nil
1L/NS
20 units IM or 5u. As bolus&
5u./hr
100/50
10:00 aM

550


o.5L/hr N.S
5u./hr
110/6o
11:00 aM
4
490
100cc
0.5l/hr+20mEq K+
5
110/60
12:00

450
400
0.5l N.S+20K+
6
120/80
1:00pm
4.5
350
600
=
6
120/80
2:00pm


250

0.5 G.W/3hr

+20mEq k
5
=
3:00pm-6pm

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Insulin Therapy:
Using soluble (Short acting) insulin administered either:
I.V infusion(prefered method):
Bolus: 0.1 unit/ kg. I.V direct
then maintain contiueous iv infusion of 0.1 unit/ kg./ hr. using syringe pump.
I.M:
Bolus: 10-20 units
Followed by 5 units hourly.

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Target blood sugar:
Falling 55-110 mg/ dl per hr.
(3-6 mmol/l)
Rapid decline → cerebral edema
Failure to reach the target → require reassessment of insulin therapy.
Shift to subcutaneous insulin regimen when the patient vomiting stopped and become biochemically stable.


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Fluid Replacement:
Average of 6 litres fluid deficit exist
3 L are extracellular replaced by 0.9% isotonic saline.
3 L are intracellular replaced by dextrose

Timing and amount as following:

1st hr: using normal (isotonic) saline
systolic BP > 90 mmHg → 1 L
systolic BP < 90 mmHg → 2 L
Set 2 wide bore IV line initially

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Then as :
1 L OVER 2 hrs
1 L OVER 2 hrs
1 L EVERY 6 hrs

Shift to 10% dextrose fluid whenever blood sugar level become < 250 mg/dl (14mmol/l).

Note: be cautious with elderly, pregnant, those with heart or renal failure.

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Potassium Replacememt
According to serum potassium level as:
> 5.5 mmol/l → non to be given
3.5 – 5.5 (mmol/l) → 40 meq/l

be cautious in replacing K usually hyperkalemia occurs initially due to prerenal failure secondary to dehydration for that reason K is not recommended to be given in the first hour of therapy.

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Other
Acidosis: is usually corrected with the time by adequate fluid and insulin replacement. Bicarbonate therapy is not recommended as it can induce cerebral edema
Infection: should be treated by antibiotcs accordingly
Brain edema: is the leading cause of death in DKA, it can exist in spite of metabolic stablisation. It should be treated by mannitol solution 20%
(7 ml/ kg.)

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Case Scenario
A 20-year-old woman is evaluated in the emergency department for polyuria, polydipsia, polyphagia, and an unintentional 5.4-kg (11.9-lb) weight loss over the past month. She has had increasing lethargy over the last 24 hours. Her medical history and family history are unremarkable. She takes no medications.

8/21/2016

On physical examination,
temperature is 37.5 °C , blood pressure is 98/52 mm Hg, pulse rate is 120/min, and respiration rate is 30/min. BMI is 17.
She is lethargic with dry mucous membranes, tachypnea, and tachycardia. Chest auscultation is clear. Abdominal examination shows diffuse mild tenderness and normal bowel sounds. There is no rebound tenderness or guarding with palpation.


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Laboratory studies:

Hemoglobin= 17 g/dL (170 g/L)
Leukocyte count= 14,200/µL (14.2 × 109/L)
Blood gases, arterial::
pH= 7.25
PCO2= 21 mm Hg
Creatinine= 1.3 mg/dL
Electrolytes
Sodium= 130 mEq/L
Potassium= 3.0 mEq/L
Chloride= 99 mEq/L
Bicarbonate= 9 mEq/L
Glucose= 620 mg/dL (34.4 mmol/L)

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An electrocardiogram shows sinus tachycardia 120/min.
Chest radiograph is normal.


What is the most appropriate management?

Hypoglycemia

Means blood glucose level < 63 mg/ dl (3.5 mmol/l) which is a common complication in diabetes [ those on insulin therapy or on oral insulin secretagoues especially sulphonylurea as Glibenclimide].
Risk factors:
1- strict glycemic control
2- extreme of age( elderly & young)
3- renal impairment
4- impaired awareness of hypoglycemia
5- long duration of DM
6- pevious history of hypoglycemia
7-ESRF (bz of insulin retention)

Causes:

1- missed or inadequate meal
2- error in therapy or poorly designed regimen
3- exercise
4- alcohol
5- lipohypertrophy at site of insulin injection.
6- factitious
7- breastfeeding


Clinical presentation:
• Autonomic symptoms: sweating, hunger, anxiety, trembling.
• Neuroglycopenic symptoms: confusion, inability to concentrate, drowsiness, incoordination, slurring of speech, coma.
• Non specific: nausea, headache
• Nocturnal hypoglycemia is common and usually not awake the person, described as poor sleep, morning headache, vivid dreams. The partner may notice sweating, twitching and seizure. It can be fatal in rare cases ( dead-in-bed syndrome)

Spontaneous hypoglycemia

• means hypoglycemia that exist in non diabetic person (uncommon condition).
• ---------------------------------------
• Any Hypoglycemia can be Confirmed by whipple s criteria:
• Assessed by doing serum insulin & C-peptide level.

Management of Hypoglycemia:

Mild cases: oral 10-15 gm. Glucose followed by snack of complex carbohydrate content.
Severe cases:
1- I.V hypertonic glucose 50% (30 ml) or 70 ml 20 %
2- I.M glucagon 1 mg
3- if the patient is conscious; 25 gm of oral refined sugar.

if the patient fail to respond

so we should exclude:
1- cerebral edema
2- alcohol intoxicaion
3- post ictal state
4- cerebral hemorrhage

Adrenal insufficiency

Secondary (↓ACTH)

Withdrawal of suppressive glucocorticoid therapy

• Hypothalamic or pituitary disease

Primary (↑ACTH)

• Intra-adrenal haemorrhage
• (Waterhouse–
• Friedrichsen syndrome
• following meningococcal
• septicaemia)
• Amyloidosis
• Haemochromatosis
• Corticosteroid biosynthetic enzyme defects
• Congenital adrenal hyperplasias
• Drugs
• (Metyrapone, ketoconazole, etomidate)
Addison’s disease
Common causes
Autoimmune
Sporadic
Polyglandular syndromes
(p. 795)
Tuberculosis
HIV/AIDS
Metastatic carcinoma
Bilateral adrenalectomy
Rare causes
Lymphoma

Clinical presentation of adrenal crisis:

presence of intercurrent infection, or surgery.
severe hypotension
Na ↓, K ↑, Ca ↑
hypoglycemia
muscle cramp
nausea, vomiting , diarrhea
unexplained fever

Investigations:

random plasma cortisol
short synacthin test

Management:

volume replacement by isotonic saline to correct hyponatremia, and hyperkalemia
hydrocortisone 100 mg I.V, then 50-100 mg every 6 hrs. till the patient tolerate oral steroid
correct hypoglycemia
Correct any underlying cause.


Thyrotoxic crisis:

is a rare life threatening condition, usually result from infection of a previously unrecognised or inadeqately treated hyperthyroid state.

Presentation:

Fever
Tachycardia or atrial fibrillation
Agitation or confusion
Acute heart failure

Management:

1- rehydration
2- propranolol 80 mg * 4 orally OR 1-5 mg * 4 I.V
3- sodium ipodate
4- Lugol s solution ( k iodide)
5- dexamethasone 2 mg * 4
6- carbimazole 40-60 mg/ day

Myxoedema coma:

• is a rare and fatal condition of old age. Usually patient present with disturb level of consciousness with severe hypothermia ( as low as 25 C), and convulsions.
Treatment:
1- I.V triiodothyronine ( T 3)… later by levothyroxine 50 Mg
2- rewarming
3- hydrocortisone


Sheehan syndrome(Hypopituitarism)

one of the commonest causes of panhypopituitarism, which occur as a result of postpartum hemorrhage.
During pregnancy the pituitary gland enlarges, so when bleeding exist the hypophyseal vessele constrict (vasospasm) causing necrosis of the pituitary gland.

Clinical presentation:

1- first symptom is inability of breast feeding
2- adrenal insufficiency
3- hypothyroidism
4- amenorrhea
5- diabetes insipidus
6- pallor ?

Management:

1- Cortisol replacement: H.C 15- 20 mg / day
2- Thyroxine 50-150 Mg / day
3- Sex hormone replacement for those below 50 years