Nursing management of Acute complications of diabetes

1. ROLE OF NURSE IN
MANAGING ACUTE
COMPLICATIONS OF
DIABETES MELLITUS
BY
MRS. R. JEYADEEPA M.SC (Nsg), MBA, PGDHM, (Ph.D)
VICE PRINCIPAL
KARUNA COLLEGE OF NURSING
VILAYODI, CHITTUR, PALAKKAD

2. LEARNING OBJECTIVES
At the end of the session participants
 Identify the impact of diabetes
 Explain the complications of diabetes
 List the diagnostic measures and s/s
 Enumerate the acute and chronic
complications
 Differentiate hyper and hypoglycemia
 Discuss the role of nurse in managing
complications
 State the measures to prevent complications
 Recognize the need for change

3. INTRODUCTION
“ MANTOSAAHAM ATHISTHOOLAM
ATHISNIGDHAM MAHASAM
MRITHYUPRAMEHA ROOPENA
KSHITRIPRA MADHYA GACHOTI”
- CHARAKA

5. IMPACT OF DIABETES
• India is the Diabetic capital of the World
• 62 millions are affected now
• 1 million deaths every year
• Prevalence in Kerala
– Overall – 15%
– Thiruvananthapuram – 16%
– Ernakulam – 20%
PRE DIABETICS ?

6. BURDEN OF DIABETES RELATED
COMPLICATIONS IN INDIA
NON DIABETIC DIABETIC
OVERALL
MORTALITY
5.3% 18.9%
CARDIO
VASCULAR
CAUSES
24.2% 52.9%
RENAL CAUSES 6.1% 23.5%

7. FACT ABOUT INDIAN DIABETICS
54% HAVE ATLEAST ONE
COMPLICATION
BECAUSE OF POOR
BLOOD SUGAR
CONTROL

8. COMLICATIONS
ACUTE COMPLICATIONS
CHRONIC COMPLICATIONS
PSYCHOLOGICAL COMPLICATIONS
SOCIO ECONOMIC COMPICATIONS

9. ACUTE COMPLICATIONS
I. HYPER GLYCEMIA
– DIABETIC KETOACIDOSIS
– NON KETOTIC HYPERGLYCEMIC HYPEROSMOLAR
DIABETIC COMA
– LACTIC ACIDOSIS
II. HYPOGLYCEMIA
III. DAWN PHENOMENON
IV. SOMOGYI PHENOMENON

10. HYPERGLYCEMIA
CAUSES
• Not enough insulin
• Too much food
• Infection, fever and illness
• Emotional stress

11. HYPERGLYCEMIA
• WATCH FOR
– Increased thirst and urination
– Large amount of sugar in blood
– Ketones in urine
– Weakness, stomach pain, general aches
– Heavy laboured breathing
– Loss of appetite and vomiting
– Fatigue
– Blurred vision, incontinence, fruity odour breath

12. HYPERGLYCEMIA
• WHAT TO DO
– Call doctor immediately
– Drink fluids without sugar if able to swallow
– Test blood sugar frequently
– Test urine for ketones if blood sugar is greater
than 240 mg/dl
– If using an insulin pump change the infusion set,
reservoir and insulin
– Give regular insulin via insulin syringe as
prescribed

13. HYPOGLYCEMIA
• CAUSES
– Too much insulin
– Not eating enough food
– Unusual amount of exercise
– Delayed meal
– Drinking alcohol without eating food
SYMPTOMS
OCCUR QUICKLY
WITHIN
MINUTES

14. HYPOGLYCEMIA MAY HAVE
DANGEROUS
CONSEQUENCES IN
CERTAIN CIRCUMSTANCES
ESPECIALLY WHILE
DRIVING

15. HYPOGLYCEMIA
• WATCH FOR
– Cold, sweat, faintness, dizziness
– Head ache
– Pounding of heart, trembling, nervousness
– Blurred vision
– Hunger
– Irritability
– Personality change
– Not able to awaken
EARLY MORING
HEADACHE IS A
COMMON SYMPTOM OF
HYPOGLYCEMIA

16. HYPOGLYCEMIA
• WHAT TO DO
– Check blood sugar level
– Take glucose tablets, food or liquid containing
sugar
– Wait for 15 minutes and recheck the blood sugar
– If still less follow the next meal
– Do not give anything by mouth if not conscious
– If unconscious give glucogon as prescribed
– Report all moderate and severe reactions to
doctor

17. The 15-15 Rule
• Give 15 grams of fast-
acting carbohydrate and
wait 15 minutes
• Recheck blood glucose
and then give another
15 grams of fast-acting
carbohydrate, if
necessary
17

18. 15 Grams of Carbohydrate Raises
Blood Glucose by 30-50 mg/dL
• 1 tube oral glucose gel
• 3-4 glucose tablets*
• ½ cup juice
• 1 tablespoon sugar,
honey, or jelly
• 8 oz milk
* Glucose tablets may contain 4 or 5 g of glucose
18

19. Treating Hypoglycemia When the
Patient Can Swallow
• 15-gram glucose
tube or 3-4 glucose
tablets*
• 4 oz fruit juice
• 8 oz milk
* Glucose tablets may contain 4 or 5 g of glucose
19

20. NURSING MANAGEMENT
• Target blood glucose is 70 to 110 mg/dl
• Ensure patent airway
• Administer liquids that contain glucose
• If the patient is alert give juice with sugar
added followed by protein and complex CHO
• If patient has decreased LOC, establish large
bore IV line and administer 50ml of 50%
dextrose as a bolus. If the consciousness is not
regained repeat the bolus

21. NURSING MANAGEMENT
• If IV access can’t be established administer
glucose gel under the tongue or give glucose
rich liquids by NG tube instead of IM dextrose
solution
• If none of the intervention is possible
administer glucogon or epinephrine IM
• Repeat blood glucose measurement in one hour
• Monitor HR, rhythm and BP.

22. NURSING MANAGEMENT
• Administer NS bolus if hypotension occurs
• Replace electrolytes based on lab results
• Determine the cause of hypoglycemia
– Poor food intake
– Change in medications
– Alcohol or other recreational drugs
– Hepatic or renal impairment
– Pancreatic tumor or endocrine disorders
– Beware of postprandial hypoglycemia

23. PATIENT TEACHING
• Teach to determine the cause and measures
to prevent it
• Teach to recognize early signs of hypoglycemia
• Teach how to use glucometer
• Emphasize the importance of having glucose
tablets, hard candy or other food containing
simple sugars readily available.

24. Diabetes control and
complications trial research
group (DCCT, 1993) and
UK prospective diabetes
study group ( UKPDS,
1998) found that the
consequences of
hypoglycemia adversely
affects the quality of life.

25. 1.DIABETIC KETOACIDOSIS
2.HYPERGLYCEMIC HYPER
OSMOLAR SYNDROME

26. HHS and DKA should be viewed as a
similar disease process with the
fundamental difference in the
metabolism on lipids during a
period of relative insulin deficiency

27. DIABETIC KETOACIDOSIS
DEFINITION
A life threatening state
that results from a relative
or absolute deficiency of
insulin

28. DKA – BIOMEDICAL TRIAD
HYPERGLYCEMIA
KETONAEMIA
METABOLIC
ACIDOSIS

29. DIABETIC KETOACIDOSIS
• Precipitating factors
– Newly diagnosed diabetes ( presenting manifestations)
– Insufficient or no insulin
– Physical stress, dehydration, trauma
– Intercurrent infection ( Pneumonia, Cholecystis)
– Vascular disoreders ( MI, Stroke)
– Endocrine disorders ( Hypothyroidism,
Pheochromocytoma)
– Trauma, Pregnancy, Surgery, etc

30. DIABETIC KETOACIDOSIS
• SIGNS AND SYMPTOMS
• Hyperglycemia
– Polyuria and polydipsia
– Severe volume depletion
– Electrolyte depletion
– Eventual: Renal hypoperfusion, prerenal azotemia,
hypotension and shock

31. DIABETIC KETOACIDOSIS
• SIGNS AND SYMPTOMS
• Ketones
– Acidosis
– Compensatory respiratory alkalosis
– Hypotension
– Shock DKA DOES NOT CAUSE
FEVER. IF FEVER IS
PRESENT, ASSUME THERE
IS AN INFECTION

32. LAB INVESTIGATIONS
• Venous blood glucose
• Electrolytes, urea, creatinine, osmolarity and
ketones
• Urine for ketones
• Blood test for infection markers
• Venous blood gas values
• Complete blood count
• Blood cultures
• Cardiac enzymes
• ECG

33. CRITERIA FOR HIGH DEPENDENCY CARE
• Blood ketones >6mmol/L
• Bicarbonate level <5mmol/L
• Venous/arterial blood gas <7.0
• Hypokalemia on admission
• GCS < 12
• Oxygen saturation < 92% on air
• Systolic BP <90mmHg
• Pulse rate >100

34. DIABETIC KETOACIDOSIS
The goals of therapy include:
1. Restoring circulatory volume
2. Insulin therapy ( Fixed rate IV Insulin infusion)
3. Correcting metabolic acidosis and electrolyte
imbalance
4. Identifying and treating precipitating factors
5. Early involvement of the diabetes specialist
team

35. RESTORING CIRCULATORY VOLUME
• AIM
– Restore circulatory volume
– Clear ketones
– Correct electrolyte imbalance
Use pulse and
BP to assess
dehydration
NS is recommended for fluid
resuscitation.
500ml to 1L rapid initial
infusion
Special attention to old age,
pregnant women, children,
young people, heart and
kidney failure.

36. FLUID BALANCE
• Daily body weight ( 1Kg increase = 1L
fluid)
•Increased JVP indicates fluid overload
•Orthostatic hypotension is the
indicator of volume depletion

37. INSULIN THERAPY
• AIM
– Reduce blood sugar
– Correct electrolyte imbalance
Insulin increases
peripheral use and
decreases hepatic glucose
production and decreases
blood glucose
concentration.
Inhibits the release of free
fatty acids from adipose
tissues and decreases
ketogenesis.

38. INSULIN SOLUTION
This solution can be prepared in such way:
50 units of insulin have to be added to a 500
ml bottle with 0.9 % sodium chloride solution,
and as a result each 10 ml of solution will
contain 1 Unit of insulin.

39. INSULIN THERAPY
• Continuous fixed rate of IV infusion of 0.1 units/kg/hr is
recommended
• 50 units of human soluble insulin made up with 50ml NS
• Infusion should continue until DKA is resolved.
• When the patient is able to eat and drink, an appropriate
subcutaneous insulin regimen should be recommended.
• Background insulin should be continued with IV infusion before
discontinue to reduce rebound hyperglycemia.
• S/C short acting insulin should be given at meal and then
discontinue IV insulin 1 hour later

40. Correcting metabolic acidosis and
electrolyte imbalance
• Targets
– Reduction in blood ketones of atleast 0.5mmol/L/hr
– Increase in venous bicarbonate by 3mmol/L/hr
– Reduction in capillary blood glucose by 3mmol/L/hr
– Maintenance of serum potassium at 4 – 5.5 mmol/L
If metabolic targets are not achieved, the rate of IV insulin
should be increased by 1 unit every hour until metabolic targets
are achieved

41. POTASSIUM
• Aim
– Maintaining normal potassium
– Prevention of hypoglycemia Both Hypo and
hyper kalemia
are life
threatening
conditions
LEAD II ECG
• Tall t waves ( Hyperkaleamia)
•Flat t wave and u wave
( Hypokalemia)
Watch for renal function before starting K replacement

42. At the time of admission K level is high but falls
with insulin treatment. So regular monitoring is
essential
Hyporeflexia and ileus are clinical
indications of potassium deficiency

43. HYPOKALEMIA
DISTURBED HEART
RHYTHM
ILEUS
WEAKNESS & PARALYSES
OF INTERCOSTAL
MUSCLES
HYPOKALEMICCOMA

44. Serum
potassium level
Potassium
deficiency
2 % potassium
solution
< 3 mmol/l 3 gr. 150 ml
3 – 4 mmol/l 2 gr. 100 ml
4 – 5 mmol/l 1,5 gr. 75 ml
5 – 6 mmol/l 1 gr. 50 ml
> 6mmol/l - -
Correction of potassium balance

45. PHOSPHATE
• Phosphate deficiency can be treated by
potassium phosphate, magnesium deficiency
can be treated by 10 % solution of MgSO4
prescription (6 – 8 ml each 3 hour under the
control of blood pressure).

46. METABOLIC ACIDOSIS
• The use of bicarbonate can be recommended
only in the following cases:
• - if life-threatening hyperkalemia;
• - when severe lactic acidosis complicates DKA;
• - with severe acidosis (pH<7), especially when
complicated by shock that is not responsive to
appropriate fluid resuscitative measures in an
attempt to improve cardiac output.
• Bicarbonate would be to infuse at a rate of 100 to
300 ml of 2,5 % solution.

47. Prevention of hypokalemia
can be made by intravenous
dropy infusion of 50 – 75 ml
2% potassium chloride solution
on each 100 mmol of
bicarbonate.

48. Capillary blood glucose
• Bed side glucose monitoring Q 1 – 2
• Dextrose infusions to stabilize blood glucose
levels ( along with NS to correct circulatory
volume)
• Monitor fluid and electrolyte balance
• Watch for cerebral edema and fluid overload
Prevention of
hypoglycemia is
vital

49. MONITOR THE PATIENT
BOTH CLINICALLY AND
CHEMICALLY

50. NURSES ROLE
• Ongoing clinical assessment
• Accurate monitoring of fluid balance
• Regular monitoring capillary blood glucose
• Monitoring of metabolic acidosis and
electrolytes
• Support early reference to diabetes team
• Provide psychological support
• Patient education on sick day management
and follow up.

51. NURSES ROLE
• Vital signs Every 15 minutes
• Record urine output, temperature and mental
status every hour
• CVP (If placed) once in every 15 minutes
• Airway patency, Level of consciousness,
hydration, status of fluid and electrolytes and
blood glucose

52. 1. NG TUBE
2. URINARY CATHETER

53. Acidosis
Lab values
Insulin
Volume replacement
Etiologies of DKA

54. COMPLICAIONS IN DKA
MANAGEMENT
COMPLICATION CAUSE COMMENTS
Hypoglycemia Insulin administration 1. Low dose insulin
2. Hourly blood glucose
monitoring, add 10% dextrose
Hyperglycemia Interruption of insulin
coverage
1. S/C insulin with infusion
2. Pre meal short acting insulin
Hypokalemia Insulin administration 1. Q2H K monitoring
2. K supplements to IV fluids
Fluid overload IV fluid Maintain fluid balance chart
Cerebral edema Rapid correction of
hyperosmolarity
1. Check Na and osmolarity Q2H
Thromboembolis Hypercoagulable state and
dehydration
Limited evidence to support
prophylactic anticoagualtion
Hypoxia/ Acute
respiratory
syndrome
Decreased osmotic pressure Add 10% dextrose when glucose is
<14mmol/L

55. OTHER THERAPEUTIC CONSIDERATION
• INFECTION
• VASCULAR THROMBOSIS – Heparine 5000
units Q4H
• VASCULAR COLLAPSE – Mesatone 1 – 2 ml,
glucocorticoides
• Cerebral edema

56. Diet – Exclusion
of fat and high
calories and CHO

57. PATIENT EDUCATION
• Frequency of blood glucose monitoring
• Blood glucose targets
• Checking for ketones
• Taking extra quick acting insulin
• Appropriate adjustment of insulin doses
• Identifying early signs and symptoms
• When to contact the physician

58. PATIENT TEACHING
• Self monitoring of blood glucose
• Urine ketone levels if blood gluocse level
exceeds 300 mg/dl
• Minimize the risk of dehydration (240 to 360
ml calorie and caffeine free liquids every hour)
• Minimize starvation ketosis by intake of
150gm CHO daily

59. WHEN TO CONSULT?
• Blood glucose > 250mg/dl
• Unable to take food or fluid

60. HHS …. Formerly known as
• Non ketotic hyperglycemic coma
• Hyperosmolar hyper glycemic non ketotic
syndrome
• Hyperosmotic non ketotic state
• Hyperglycemic hyper osmolar syndrome

61. Nonketonic hyperglycemic-hyperosmolar coma
(NKHHC or HNC).
HNC is a syndrome characterized by impaired
consciousness, sometimes accompanied by
seizures, extreme dehydration, , and extreme
hyperglycemia that is not accompanied by
ketoacidosis.q

62. HHS
USUALLY DEVELOPS AFTER A PERIOD OF
SYMPTOMATIC HYPERGLYCEMIA IN
WHICH FLUID UNTAKE IS INADEQUATE TO
PREVENT EXTREME DEHYDRATION FROM
THE HYPERGLYCEMIA INDUCED OSMOTIC
DIURESIS

63. Predisposing factors
1. HNC seems to occur spontaneously in about 5 – 7 % of patients.
2. Infection (e.g., pneumonia, urinary tract infection, gram-negative
sepsis) is underlying frequent precipitating cause.
3. Use of certain drugs has been associated with this condition:
• steroids increase glucogenesis and antagonize the action of
insulin;
• potassium-wasting diuretics (hypokalemia decreases insulin
secretion), e.g., thiazides, furosemide;
• other drugs, e.g., propranolol, azathioprine, diazoxide.
5. Other medical conditions such as cerebrovascular accident,
subdural hematoma, acute pancreatitis, and severe burns have
been associated with HNC.
6. Use of concentrated glucose solutions, such as used in peripheral
hyperalimentation or renal dialysis, has been associated with
HNC.
7. HNC can be induced by peritoneal or hemodialysis, tube feeding.

64. SIGNS AND SYMPTOMS
• Polyuria, polydipsia, weight loss, weakness
and progressive changes in the state of
consciousness.
• Consider other causes of coma in old age
• Seizures occur in 5% of patients

65. Physical examination
1. Severe dehydration is invariably present.
2. Various neurologic deficits (such as coma, transient
hemiparesis, hyperreflexia, and generalized areflexia)
are commonly present. Altered states of
consciousness from lethargy to coma are observed.
3. Findings associated with coexisting medical
problems (e.g., renal disease, cardiovascular disease)
may be evident.

66. Laboratory findings
1. Extreme hyperglycemia (blood glucose levels from 30
mmoll/l and over are common.
2. A markedly elevated serum osmolality is present, usually in
excess of 350 mOsm/l. (Normal = 290 mOsm/l).
3. The initial plasma bicarbonate averaged.
4. Serum ketones are usually not detectable, and patients are
not acidic.
5. Serum sodium may be high (if severe degree of dehydration
is present), normal, or high (when the marked shift of water
from the intracellular to the extracellular space due to the
marked hyperglycemia is present).
6. Serum potassium levels may be high (secondary to the
effects of hyperosmolality as it draws potassium from the
cells), normal, or low (from marked urinary losses from the
osmotic diuresis). But potassium deficiency exists.

67. Treatment
This condition is a medical emergency and the
patient should be placed in an intensive care unit.
Many of the management techniques
recommended for a patient with DKA are
applicable here as well.

68. GOALS OF
THERAPY
REHYDRATION
REDUCTION
OF
HYPERGLYC
EMIA
ELECTROLYTE
CORRECTION
TREATMETNT
FOR THE
CAUSE

69. REHYDRATION
• Average fluid deficit is 10 lt
• Acute circulatory collapse is a common
terminal event
• Too rapid correction of hyperglycemia
Hypovolemic shock ( Fluid shift from
extra cellular space to intra cellular space)

70. REHYDRATION
• 1 – 2 lt of 9% Nacl for 1 – 2 hours
• 0.45% Nacl @150 to 500ml/hr depending on
the state of hydration
• Half of the fluid loss is replaced in the first 12
hours rest in subsequent 24 hours
Aim is not to correct the deficit
rapidly rather to maintain stable
circulation and renal function

71. NURSES ROLE
• Monitors signs and symptoms of HNC
• Ongoing assessment of fluid status
• Determine the rate of fluid administration by
assessing weight, urine output, kidney function,
pulmonary congestion & JVP
• CVP monitoring if the patient is a known case of
CCF, Renal insufficiency or ARF
• Assess for signs of cerebral edema every hour
• Assess LOC, Pupil size, shape and reaction
• Assess for seizures and report any abnormality
immediately

72. INSULIN THERAPY
• 10 -20 units of regular insulin IV bolus
followed by infusion in a dose of 0.05 – 0.10
units/kg/hour
• When desirable blood glucose level is
achieved, 5% dextrose is added to prevent
hypoglycemia
Insulin aggravates existing
hypotension and oliguria. So in some
cases insulin administration is
delayed till vital signs are stable by
NS

73. CORRECTION OF ELECTROLYTES
• Once urine flow has been reestablished K
should be added
• Add 20mmol/l K in 0.45% Nacl with careful K
and ECG monitoring

74. Lactic acidosis (LA).
DM is one of the major causes of LA, a serious condition
characterized by excessive accumulation of lactic acid
and metabolic acidosis.
The hallmark of LA is the presence of tissue hypoxemia,
which leads to enhanced anaerobic glycolysis and to
increased lactic acid formation.
The normal blood lactic acid concentration is 1mmol/l,
and the pyruvic to lactic ratio is 10:1. An increase in
lactic acid without concomitant rise in pyruvate leads
to LA of clinical importance.

75. Predisposing factors
1. Heart and pulmonary failure (which leads to hypoxia).
2. Usage of bigyanids, pheformin therapy.
3. Alcohol intoxication.
4. Ketoacidosis (it is important to have a very high index
of suspection with respect to presence of LA).

76. SIGNS AND SYMPTOMS
• Kussmaul breathing ( due to respiratory
compensation of metabolic acidosis)
• Headache, drowsiness & lassitude
• Anorexia, Nausea, Vomiting and abdominal
pain
• Myalgia

77. Physical examination
1. Acrocyanosis is common.
2. Tachycardia frequently is present, blood pressure is
decreased.
3. Poor skin tugor and dry skin may be prominent.
4. Hypothermia is common in LA.
5. Hyperpnea or Kussmaul respiration are present and
related to degree of acidosis.
6. Findings associated with coexisting medical problems
(e.g., renal disease, cardiovascular disease) may be
evident.

78. Laboratory findings
1. Blood glucose level is not high
2. Glucosurea is absent.
3. Blood lactic acid is high.

79. Treatment of LA
LA is treated by correcting the underlying cause.
Oxygentherapy
Metylen blue (50 – 100 ml of 1 % solution i/v droply)
In severe cases, bicarbonate therapy should be used
(intravenously-infused 2,5 % sodium bicarbonates 1 to 2
l/day).
LA can be treated with low dose insulin regimens with 5 %
glucose solution infusion.
Symptomatic therapy:
- Hydrocortisone (250 mg i/v)
- Unitiol (5% solution 10 ml i/v (1- 2 ml/10 kg)
- α-lipoid acid (berlition, espa-lipon)

80. Comparison of DCA, HNC and LA.

81. DAWN PHENOMENON
• Abnormally high plasma glucose levels in
morning before breakfast. (Between 3am to
5am)
MORE COMMON
WITH PEOPLE
WITH POOR
GLYCEMIC
CONTROL

82. GH, CORTISOL &
CATECHOLAMINES
RELEASE OF
SUGAR FROM
LIVER
HYPERGLYCEMIA

83. PREVENTION
• Increasing evening physical activity
• Increasing protein to CHO ratio in the last
meal of the day and the breakfast
• Diet modification
• Increase bedtime dose of hypoglycemic agents
with night time peaks of action
• Continuous subcutaneous insulin infusion

84. SOMOGYI EFFECT
In 1930, Dr. Michael somogyi speculated that
hypoglycemia during the late evening induced
by insulin could cause a counter regulatory
hormone response that produces
hyperglycemia in the early morning.
PROBABLY OCCURS WITH
TYPE I AND LESS
COMMON IN TYPE II

85. TREATMENT
• Substitution of regular insulin with immediate
acting insulin
• Continue glucose monitoring with special
attention to somogyi phenomenon

86. Moghissi ES, et al. Endocrine Pract. 2009;15:353-369.
Umpierrez GE, et al. J Clin Endocrinol Metab. 2012;97:16-38.
Inpatient Glycemic Control
Recommendations
• Identify elevated blood glucose in all hospitalized
patients
• Implement structured protocols for control of blood
glucose throughout the hospital
– Glucose targets:
• ICU: 140-180 mg/dL for most patients
• Noncritically ill: Fasting BG <140 mg/dL; random BG <180 mg/dL
• Create educational programs for all hospital personnel
caring for people with diabetes
• Plan for a smooth transition to outpatient care with
appropriate diabetes management
86

87. Glucose Control Deteriorates
During Hospitalization
Hyperglycemic Influences
• “Stress” hyperglycemia
• Concomitant therapy
• Decreased physical activity
• Medication omissions
• Medication errors
• Fear of hypoglycemia
Hypoglycemic Influences
• Decreased caloric intake
• Gastrointestinal illness
• Monitored compliance
• Medication errors
• Altered cognition
Metchick LN, et al. Am J Med. 2002;113:317-323.
87

88. What Is the Impact of NPO Status on
the Patient’s Blood Glucose Levels?
• Ideally, patients will have surgery early in the
morning to avoid a prolonged NPO period
• NPO patients need regular blood glucose
monitoring (every 4-6 hours) and may need IV
fluid
• NPO patients on oral diabetic medications
with long duration are at risk for hypoglycemia
88

89. NPO Patients
• Management differs for type 1 and type 2
– Type 1 patients still need basal insulin
• Transport with insulin on board
• Advocate for early test procedures so patients
do not miss too many meals
• Solution: use insulin analogs for basal/bolus
89

90. NPO Patients
• May give half of the basal insulin dose, hold
the mealtime insulin, and continue the
correction dose
• Monitor BG every 6 hours and give corrective
insulin as needed
• Resume the previous regimen once the
patient is eating again
90

91. What Is the Impact of Tube Feedings
on Blood Glucose Levels?
• Patients on tube feedings will usually receive a
continuous flow of carbohydrates via their
feeding
• Blood glucose monitoring (usually every 4 or 6
hours) and scheduled dose of insulin plus
corrections are needed
• Interruption of feeding can cause hypoglycemia
– IV dextrose may be needed while the feeding is off
– Notify physician for IV dextrose and adjustment of
insulin orders when there is interruption or change
in feeding rate
91

92. Nursing Role in Good Glycemic
Control
• Point of care testing (POCT) for all patients
with diabetes and patients who present with
hyperglycemia on admission
• Special situations that cause hyperglycemia
– Steroids
– Immunosuppressants (eg, cyclosporin)
– Atypical antipsychotics
• Enteral nutrition or total parenteral nutrition
(TPN)
• Start POCT without an order—need guideline
for care or policy
92

93. Nursing Role in Good Glycemic
Control
• Appropriate timing of point of care
testing/insulin administration and meal
delivery
– Document capillary blood glucose and the time
– Document insulin dose and the time given
– Document percentage of the carbohydrate eaten
93

94. Nursing Role in Good Glycemic
Control
• Appropriate timing of PCT/insulin
administration and meal delivery
– Document FS blood glucose and the time
– Document insulin dose and the time given
– Document percentage of the carbohydrate eaten
Do not hold insulin just because blood glucose is
under good control!
94

95. Nursing Role in Good Glycemic
Control
• Appropriate patient handoff when transferring
patient to another area of the hospital
– Meal plan order
– Last capillary glucose level
– Insulin dose and last insulin given
– Patient teaching done and patient’s response
– Identified further educational needs of
patient/family
– Transport sheet
95

96. 1.PSYCHOSOCIAL COMPLICATIONS
2.ECONOMIC COMPLICATIONS

97. ROLE OF A NURSE
EMPHASIS ON SELF
MANAGEMENT

98. Enable people to active
participants and
decision makers not a
passive recipients of
health care

99. NURSES ARE
NOT THE FIRST
INFORMATION
GIVERS

100. 1.WORK TOWARDS THE OBJECTIVES
2.TARGET SETTING
3.DETERMINING PRIORITIES
4.MEASURES TO PREVENT COMPLICATIONS
5.IF DO APPEAR PREVENT FROM WORSENING
GLYCEMIC CONTROL

101. 1. TARGET HbA1c
2. BP control ( less than 140/100
mmhg)
3. Cholestrol ( Total < 5mmol/l, HDL
>1, LDL <3
4. Screening for comolications
5. Nutrition advice

102. Living with diabetes is like
living with a tiger. If you
feed it, groom it, never
turn your back on it; you
can live with a tiger.
If you neglect it; it will
pounce on you rip you to
shreds

105. THANK YOU