PATIENT WITH

ENDOCRINE
DYSFUNCTION
Diabetic
emergencies
LEARNING OUTCOMES:
• 1.differentiate between the following acute diabetic emergencies:
diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic syndrome
(HHS) and hypoglycemia
• 2. correlate the clinical presentation of the above acute diabetic
emergencies with its pathophysiology
• 3. state the relevant laboratory data concerning the above acute
diabetic emergencies
• 4. describe the management related to the above acute diabetic
• emergencies
• 5. use the nursing process as a framework to formulate
individualized care of patients with the above acute diabetic
emergencies
• 6. appreciate the importance of prompt management to the
patient’s clinical prognosis
Diabetic mellitus
•a disorder of carbohydrate metabolism,
usually occurring in genetically
predisposed individuals, characterized by
inadequate production or utilization of
insulin and resulting in excessive amounts
of glucose in the blood and urine,
excessive thirst, weight loss, and in some
cases progressive destruction of small
blood vessels leading to such
complications as infections and gangrene
of the limbs or blindness.
IDDM – JUVENILE –ONSET
Type 1 – ( Diabetes Mellites )
•Also called type 1 diabetes,
insulin-dependent diabetes, juvenile
diabetes. a severe form of diabetes
mellitus in which insulin production by
the beta cells of the pancreas is impaired,
usually resulting in dependence on
externally administered insulin, the onset
of the disease typically occurring before
the age of 25.
• Insulin is a hormone produced in the pancreas by special cells,
called beta cells. The pancreas is below and behind the
stomach. Insulin is needed to move blood sugar (glucose) into
cells. Inside the cells, glucose is stored and later used for
energy. With type 1 diabetes, beta cells produce little or no
insulin.

• Without enough insulin, glucose builds up in the bloodstream

instead of going into the cells. This buildup of glucose in the
blood is called hyperglycemia. The body is unable to use the
glucose for energy. This leads to the symptoms of type 1
diabetes.
Type 2 – Diabetes Mellitis
•Also called type 2 diabetes,
non-insulin-dependent diabetes,
adult-onset diabetes, maturity-onset
diabetes. a mild, sometimes asymptomatic
form of diabetes mellitus characterized by
diminished tissue sensitivity to insulin and
sometimes by impaired beta cell function,
exacerbated by obesity and often treatable
by diet and exercise.
Diabetes Ketoacidosis (DKA)
•Is life threathing medical
emergencies
•It is characterised by
•Hypergycaemia
•Dehydration
•Metabolic acidosis
•ketonuria
Definition of Acute Diabetic
Emergencies
•DKA is a syndrome of hyperglycemia
(blood glucose >13.8 mmol/L)
•metabolic acidosis (pH <7.30, serum
bicarbonate <18 mmol/L,
• anion gap >10),
•Ketosis- presence of ketone in urine
and plsma ketones
• and severe volume depletion.
•DKA occurs mainly in insulin
dependent diabetics, and severe
insulin deficiency
•Raised serum levels of stress
hormones (glucagon,catecholamines,
cortisol, and growth hormone) are
also a feature.
Common precipating events
of DKA
1. Infections ( commonly urinary tract – 30
%)
2. 2. Non- complaince with treatment – 15
%
3. New diagnosis of type 1 diabetes – 5- 15
%
4. Other stresses
(MI,alcohol,pancreatitis,drugs)-5%
5. No causes found – 40%
Acid base Imbalance in DKA
-Hyperglysemia : when there is no insulin glucose cannot be
transported into the cell
- Therefore insulin deficiency increase the level of fatty acid is a
result to lipolysis
- these fatty acid are oxidize in the liver produce acidic ketones
bodies and thereby reduces blood Ph causes metabolic
acidosis
- Hyperglycemia produces an osmotic diuresis – increase loss of
fluids ( polyuria ) will reduce intravascular blood volume and
electrolyte lead to hyperosmolarity and dehydration –
hypoperfusion to the tissue leading to anerobic metabolism by
produce of anerobic metabolism courses formation of lactic lead
to metabolic acidosis
Clinical manifestation DKA
1. Sign of symtom of dehydration
- Reduce / poor skin turgor
- Sunken eyeballs / wrinkle cornea
- Dry mucous membranes
- Thrist / polydipsea and polyuria
- Tachycardia and hypotension

2. Polyuria ( osmotic diuresis cause by hyperglysemia

- Glycosuria
- Ketonuria > 2 + ( moderate / large )
3. Tachypnea – kussmaul respiration ( deep and fast breathing)
- deep rapid respiration to provide respiratory compensation for
metabolic acidosis
4. Ketone breath

5. Altered conciousness and confusion , lethargic,stupor, coma

6. Loss of electrolytes – phosphate sodium and pottasium

7. Acidosis Ph below 7.3 , sodium bicarbonate < 18 mEg/L

8. Nausea and vomiting

 Management
-Rehydration
-Correction of the electrolyte imbalance
and acid- base disturbance
-correction of hypoglycaemia state
- Monitoring and frequent review of
clinical sign and labarory test to detect
and treat complication
1. Volume replacement
- Establish intravenous (IV) access with at least at large gauge
branula
- Normal saline with CVP monitoring
- Plasma expender if BP low
- Administer Isotonic ( 0.9 % Normal Saline ) – rapid restoration
of the intravascular volume
- In the first hour 0.9 % bolus is given at a rate of 15-20 ml/kg
Or average of 1-2 L until SBP > 100 mmHg ,HR 110/min and
urine flow 0.5- 1 mls /kg/hr indicate the haemodynamic is stable
- If presistanly hypotensive –colloid solution
- Once BP is normalize , Sr Sodium elevated and Sr Osmalarity is
more than 320 mOsm/kg hypotonic saline 0.45 % is use to
replace intracellular fluid deficit
• When the blood glucose is 14 mmol/L the fluid should be
change to 5 % Dextrose with 0.45 % saline until the acidosis
and ketosis have resolved
• Dextron 10 may be used if Sr Glucose ≤ 8.0 mmol/L ,Ph > 7.2
Bicarbonate is > 18 mEq/L
- Monitor for adequate fluid replacement
- Monitor urine output to achieve > 0.5 ml- 1 ml /kg/hr
- Monitor strict intake and output chart
- Monitor for adequate fluid replacement
- HR 60-100 /min
- MAP > 70 mmHg
- CVP> 7 mmHg ( 8- 12 mmH g )
• Capillary refill < 3 sec
• Urine keton – ve
• Obseve sodium – 135- 145 mmol/L
• Watch for fluid overload –CVP monitoring
• Monitor haemodynamic parameter and breath sound to
detect fluid volume overload from aggressive fluid replacemnt
- Tachycardia
- Fine crackles
- Neck vein distension
- Increase CVP
2. Insulin Therapy
Once Hypokalemia has been exclude an intravenous insulin
infusion should be commanced ( 50 Ü act in 50 ml 0.9 % Normal
Saline run at 0.1 unit /kg/hr
- Rapid correction of Sr Glucose is assciated with
hypoglycemia,hypokalemia and cerebral edema
- Administer IV bolus insulin stat dose / loading dose at 10-2-
unit as oreded
- Prepared for cortinuous infusion of insulin mix 50 unit insulin
with 50 ml Normal saline
- Start infusion of insulin according to sliding scale ( eg 5-10 unit
/hr or 0.1 unit /kg/hr ) or infusion 6 unit /hr – according to
hospital protocol
Administer insulin infusion via syringe pump to ensure precise
dosage and smooth infusion
- 2 hly blood glucose monitoring while patient on continuous
infusion titrate close insulin according or target for the fall in
plasma glucose is 3-4 mmol/L /hr
- If blood glucose fail to fall at this rate the insulin rate should be
double every hour until the target is reached
- If plasma glucose fall exceeds 5 mmol/l the rate should be
reduced to 0.05 unit /kg/hr
- Monitor Sr Glucose every 6 hour
- Maintain blood glucose 8-10 mmol/L
- Monitor urine ketone till negative
• Monitor for potassium – insulin therapy can induce
- Hypokalemia
- Monitor ECG direct for sign of hypokalemia
- Observe for sign and symptom of insulin therapy – sign of
hypoglycemia ,hypotension, tachycardia, cold and clammy skin
3. Correct electrolyte
•Replacement of IV infusion KCL /add
in iv drip
•Monitor Sr electrolyte
•Check for sign of hypokalemia – U
wave on ECG
4. Correct Acidosis
•Formula used to calculate the
anion gap
•( sodium ) – ( chloride + Hco3 ) = <
15 mEq/L
•Monitor ABG & HCO3
Hypokalemia
• Monitor Sr Potassium and maintain potassium level 3.5- 4.5
mmol/L
• Monitor ECG – peak T wave ,prolonge PR ,widing QRS
• Give IV lytic cocktail as ordered by doctor
• Dextrose 50% in 50 ml and IV Insulin 10 unit – to move the
pottasium to the cell
• To calcium gluconate to protect heart and prevent from
arrthymias
• Give IV lasix to encourage diuresis
• Stop all pottasium supplement such as Tab Slow K, iv KCL
infusion
2. Hyperosmolar
hyperglycaemic
syndrome (HHS)
According to American Diabetic
Association diagnostic features of
HHS may include the following
1. Plasma glucose level of 33 mmol/L 600 mg/Dl
or greater
2. Effective serum osmolarity of 300 mOsm/kg or
greater
3. Profound dehydration ( up to an averageof 9L )
4. Serum Ph greather than 7.30
5. Bicarbonate concentration greater than 15
mEQ/L
6. Absent to small ketonemia
• 7. Neurological impairment
• Altered conscious state
• Confusion
• Seizures
• Coma
INVESTIGATION
Blood tests
1. FBE
2. UREA AND ELECTROLYTE
GLUCOSE - typically 50-60 mmol/L or higher
Correction Na level is high often 160 mmol/L
3. ABG – may show no, mild acidosis
4. High osmolarity > 320 mosmol/L
IF > 350 mosmol/ L coma may accor
5.Blood culture
6. Cardiac enzymes
• 7. ECG
As for any unwell patient
- Possible precipating acute coronary syndrome
- 8. CXR
- Possible precipating acute coronary syndrome
- 9. urine
- FEME and culture
- 10. CT scan brain
Clinical features
• Hyperosmolar hyperglycemic state (HHS) most
common with
• Type II DM
• Middle age to elderly
• Have some precipitating illness that leads to
reduced fluid intake
• A precipating illness ( most commonly infection
,ACS )
Management
• Similar to DKA
• Rehydration of patient is best achieved slowly ( to avoid risk of
cerebral edema )
• Insulin replacemnt – some modification in fluid use and rate of
insulin slow rate
• 0.5- 2 unit per hour
Nursing Care

•Problem 1: Fluid volume deficit related to

hyperglycemic induced osmotic diuresis
•Clinical assessment findings
• Decrease skin turgor
• Poor capillary refill
• Tachycardia, hypotensive
• Increase urine output
Intervention
• 1. Assess for signs of fluid volume deficit
• 2. Monitor the vital signs – mental status, heart
rate, blood pressure, peripheral perfusion and
urine output
• 3. Administer intravenous normal saline
• 4. Volume and rate of fluid infusion depends on
initial hemodynamic status and
• the respond to fluid therapy (heart rate, blood
pressure, peripheral perfusion and urine output)
•5. Administer insulin therapy at 0.05 – 0.1
unit/kg/hr
•6. Supplement with intravenous Dextrose
5% when the blood sugar drops to
15mmol/l or less
•7. Check serum electrolyte – hypokalemia,
hypophosphatemia may be present and
need to be corrected
•8. Monitor blood sugar level every
hour than reduce to 2 hourly when its
more stable
•9. Find out the precipitating cause for
DKA
Problem 2: Electrolyte
imbalance - hypokalemia
related to diuresis
•Clinical Assessment Findings
• Weakness, hypotonicity
• ECG monitor – prolongation of the PR
interval, T wave inversion and prominent U
waves
• Intervention
• 1. Assess the potassium level
• 2. Observe the ECG for evidence of cardiac arrhythmias
• 3. Administer oxygen through ventimask (to titrate FiO2
according to oxygen saturation)
• 4. Administer intravenous potassium chloride slow infusion at
a dose of not exceeding 0.5mmol/kg/hr. (Patient must be
attached to continuous ECG monitoring during the infusion)
•5. Check serum potassium serially to
see the response of treatment or
recurrent
•6. In refractory hypokalemia, check
magnesium level
•7. Control blood sugar level to stop
the diuresis