Best notes

1. Acute Complications of Diabetes
 There are three major acute complications of diabetes related to
short-term imbalances in blood glucose levels:
a. Hypoglycemia
b. Diabetic ketoacidosis/DKA, and
c. Hyperglycemic hyperosmolar non ketotic syndrome/HHNS, which
is also called hyperglycemic hyperosmolar syndrome or state

2. Hypoglycemia (Insulin Reactions)
 Occurs when the BGLs falls to < 50 to 60mg/dL (2.7 to
3.3mmol/L)
 Causes
 Too much insulin or OHAs
 Too little food
 Excessive physical activity
 Often occurs before meals, especially if meals are delayed or
snacks are omitted

3. Hypoglycemia Clinical manifestations
i. Mild hypoglycemia
 Stimulation of sympathetic nervous system resulting in a surge of
epinephrine and norepinephrine
 In turn results in:
 Sweating
 Tremor
 Tachycardia
 Palpitation
 Nervousness
 Hunger

4. Hypoglycemia C/Ms Cont’d
ii. Moderate hypoglycemia
 Drop in BGL deprives the brain cells of needed fuel for
functioning
 Signs of impaired function of the CNS may include:
 Inability to concentrate
 Head ache, Light headiness,
 Confusion, Memory loses,
 Slurred speech,
 Double vision
 Drowsiness,
 Numbness of the lips and tongue

5. Hypoglycemia C/Ms Cont’d
 Sever hypoglycemia
 Results in:
 Impaired CNS functions
 Disoriented behavior
 Seizures,
 Difficulty arousing from sleep, and
 Loss of consciousness

6. Management
A. Immediate treatment with carbohydrate
 The usual recommendation is for 15 g of a fast-acting concentrated
source of carbohydrate such as the following, given orally:
 A. Three or four commercially prepared glucose tablets
 B.100-150 ml of fruit juice or regular soda
 C.6 to 10 hard candies
 D.2 to 3 teaspoons of sugar or honey
 Nursing Alert: To prevent sharp increase in BGL, it is not
necessary to add sugar to juice, even if it is labeled as unsweetened
juice: the fruit sugar in juice contains enough carbohydrate to raise
the BGL

7. Management Immediate treatment with carbohydrate…
 The BGL should be retested in 15 minutes and retreated if it is
less than 70 to 75 mg/dL (3.8 to 4 mmol/L)
 If the symptoms persist for longer than 10 to 15 minutes after
initial treatment, the treatment is repeated
 Once the symptoms resolve, a snack containing protein and
starch (eg, milk or cheese and bananas/crackers) is recommended
unless the patient plans to eat a regular meal or snack within 30 to
60 minutes

8. Management Immediate treatment with carbohydrate…
B. Initiating Emergency Measures
 Glucagon injection:
 Has an onset of 8 to 10 minutes, and its action lasts 12 to 27 minutes
 For adults who are unconscious and cannot swallow, an injection of
glucagon 1mg can be administered either subcutaneously or
intramuscularly
 After injection of glucagon, the patient may take as long as 20
minutes to regain consciousness

9. Management Immediate treatment with carbohydrate…
 A concentrated source of carbohydrate:
 Should be given to the patient on awakening to prevent recurrence of
hypoglycemia followed by a snack
 50%/40% Dextrose in water (D50W/D40W)
 For patients who are unconscious or cannot swallow
 25 to 50 mL of 50%/40% dextrose in water may be administered IV
 The effect is usually seen within minutes

10. Cont…
 Providing Patient Education
 Consistent pattern of eating, administering insulin, and exercising
 Between-meal and bedtime snacks may be needed to counteract the
maximum insulin effect
 The patient should cover the time of peak activity of insulin by eating
a snack and by taking additional food when physical activity is
increased
 Routine blood glucose tests to anticipate change insulin requirements
and to adjust the dosage

11. Cont…
 To prevent unexpected hypoglycemia all patients treated with
insulin should wear an identification bracelet or tag stating that
they have diabetes Symptoms of hypoglycemia
 Patients with diabetes, especially those receiving insulin, learn to
carry some form of simple sugar with them at all times
 Advising to refrain from eating high-calorie, high-fat dessert
foods (eg, cookies, cakes, ice cream) to treat hypoglycemia
because their high fat content may slow the absorption of the
glucose and resolution of the hypoglycemic symptoms

12. Diabetic Ketoacidosis (DKA)
 Diabetic Ketoacidosis (DKA)
 Definition
 DKA is a metabolic derangement in T1D that is caused by an
absence or markedly inadequate amount of insulin
 Insulin deficiency results in disorders in the metabolism of
carbohydrate, protein, and fat

13. DKA Causes: Three main causes
1. Decreased or missed dose or deficiency of insulin caused by:
 An insufficient dosage of insulin prescribed
 An insufficient insulin being administered by the patient
 Patient error in drawing up or injecting insulin
 Intentional skipping of insulin doses
 Equipment problems
2. Illness or infection
3. Undiagnosed and untreated diabetes

14. DKA Causes …
 Illnesses and infections are associated with insulin resistance
 In response to physical (and emotional) stressors, there is an
increase in the level of “stress” hormones:
 Glucagon,
 Epinephrine, norepinephrine,
 Cortisol, and
 Growth hormone
 These hormones promote glucose production by the liver and
interfere with glucose utilization by muscle and fat tissue

15. DKA: Pathophysiology
The three main clinical features of DKA are:
1.Hyperglycemia
2.Dehydration and electrolyte loss
3.Acidosis

16. Pathophysiology DKA
 DKA results from relative or absolute insulin deficiency combined
with counter regulatory hormone excess (glucagon,
catecholamine's, cortisol, and growth hormone).
 Both insulin deficiency and glucagon excess, in particular, are
necessary for DKA to develop.
 The decreased ratio of insulin to glucagon promotes
gluconeogenesis, glycogenolysis, and ketone body formation in the
liver, as well as increases in substrate delivery from fat and muscle
(free fatty acids, amino acids) to the liver.
 Markers of inflammation (cytokines, C-reactive protein) are
elevated in both DKA and HHS
 The combination of insulin deficiency and hyperglycemia reduces
the hepatic level of fructose-2,6-bisphosphate, which alters the
activity of phosphofructokinase and fructose-1,6-bisphosphatase.

17.  release of free fatty acids. Normally, these free fatty acids are
converted to triglycerides or very-low-density lipoprotein
(VLDL) in the liver.
However, in DKA, hyper glucagonemia alters hepatic
metabolism
to favor ketone body formation, through activation of the enzyme
carnitine palmitoyltransferase I.
 This enzyme is crucial for regulating fatty acid transport into the
mitochondria, where beta oxidation and conversion to ketone
bodies occur. At physiologic pH, ketone bodies
exist as ketoacids, which are neutralized by bicarbonate.
 As bicarbonate stores are depleted, metabolic acidosis ensues.
Increased lactic acid production also contributes to the acidosis.

18. DKA: Diagnosis
 BGLs may vary from 300 to 800mg /dL
 Serum Bicarbonate 0-15mq/L
 PH 6.8-7.3
 PaCO2 10-30mmHg – Respiratory compensation
 Increased creatinine
 Increased BUN
 Increased hematocrite

19. DKA: Prevention
 If DKA is related to illness, teach the patient about “Sick
day” rules for managing their diabetes when ill
 Assess diabetic self management skills including blood
glucose testing and insulin administration
 If insulin dose is intentionally altered, psychological
counseling is recommended for patients and family
members

20. Cont…
1.Take insulin or oral antidiabetic agents as usual.
2.Test blood glucose and test urine ketones every 3 to 4 h.
3.Report elevated glucose levels (300 mg/dL [16.6 mmol/L] or as
otherwise specified) or urine ketones to your health care provider.
4.If you take insulin, you may need supplemental doses of regular insulin
every 3 to 4 h.
5.If you cannot follow your usual meal plan, substitute soft foods (eg, 1
cup cream soup, 1⁄2 cup custard, 3 squares graham bananas) six to eight
times per day

21. DKA Prevention: “Sick Day Rules”…
6.If vomiting, diarrhea, or fever persists, take liquids (eg, 1⁄2 cup
regular cola or orange juice, 1⁄2 cup broth, 1 cup Gatorade) every
1⁄2 to 1 hour to prevent dehydration and to provide calories.
7.Report nausea, vomiting, and diarrhea to your health care
provider, because extreme fluid loss may be dangerous.
8.If you are unable to retain oral fluids, you may require
hospitalization to avoid diabetic ketoacidosis and possibly coma

22. DKA: Medical Management
Treatment Goals:
1.Treating hyperglycemia
2.Correcting dehydration
3.Maintaining electrolyte balance
4.Reversing acidosis

24. Hyperglycemic hyperosmolar…
 Hyperglycemic hyperosmolar state(HHS) is a hyperglycemic
emregncy that occurs in type 2 DM due to relative insulin
deficiency and inadequate fluid intake.
 Occurs most often in older people (50 to 70 years of age) who
have no known history of diabetes or who have type 2 diabetes
 Except the acidosis the manifesations, risk factors and
management of HHS is similar to DKA

25. Cont…
 Hyper osmolality and hyperglycemia are predominant
 The patient’s persistent hyperglycemia causes osmotic diuresis,
resulting in losses of water and electrolytes.
 Because of water shifts from ICF space to ECF space the patient
may present with neurologic abnormalities such as:
 Somnolence, coma,
 Seizures,
 Hemiparesis, and
 Aphasia

26. Cont…
HHNS: Precipitating factors
i. Acute illness (e.g. pneumonia, stroke)
ii. Medications that exacerbate BGL (e.g. thiazides)
iii. Treatments such as dialysis

27. Pathophysiology HHS
 Relative insulin deficiency and inadequate fluid
intake are the underlying causes of HHS.
 Insulin deficiency increases hepatic glucose production (through glycogenolysis
and gluconeogenesis) and impairs glucose utilization in skeletal muscle (see
above
discussion of DKA).
 Hyperglycemia induces an osmotic diuresis that leads to intravascular volume
depletion, which is exacerbated by
inadequate fluid replacement. The absence of ketosis in HHS is not
understood.
 Presumably, the insulin deficiency is only relative and less
severe than in DKA.
 Lower levels of counter regulatory hormones and
free fatty acids have been found in HHS than in DKA in some studies.
It is also possible that the liver is less capable of ketone body synthesis
or that the insulin/glucagon ratio does not favor ketogenesis.

28. Laboratory Abnormalities and Diagnosis
 The laboratory features in HHS
 Most notable are the marked hyperglycemia (plasma glucose may
be >55.5 mmol/L [1000 mg/dL]), hyperosmolality (>350
mosmol/L), and prerenal azotemia.
 The measured serum sodium may be normal or slightly low despite
the marked hyperglycemia.
 The corrected serum sodium is usually increased (add
1.6 meq to measured sodium for each 5.6-mmol/L [100-mg/dL]
rise inthe serum glucose). In contrast to DKA, acidosis and
ketonemia areabsent or mild.
 A small anion-gap metabolic acidosis may be present
secondary to increased lactic acid.
 Moderate ketonuria, if present, is secondary to starvation

29. HHNS: Diagnosis
 History
 Physical Examination
 Lab test
 BGL 600 to 1200mg/dL
 Electrolytes
 BUN
 CBC- RBCs
 Serum osmolality >350 mosm/kg
 ABG analysis – PH normal

30. Management of DKA or HHS
The overall approach to the treatment of HHNS is similar
to that of DKA:
Fluid replacement,
Correction of electrolyte imbalances, and
Insulin administration

31. Management of DKA or HHS
 1.Replace fluids:
2–3 L of 0.9% NS in 1–3 hr; the reduce to 250–500 mL/h; change to
5% glucose
when plasma glucose reaches 250 mg/dl in DKA and 300mg/dl in
HHS. HHS requires
more fluid.Assess hydration status, BP and urine out put ferquently
Patients may need up to 6-10 liters of IV fluid per day
 Initially 0.9% NaCl – 0.5 to 1L per hour for 2 to 3hrs.
 Use 0.45% NaCl for the patients with hypertension or
hypernatremia or those at risk for heart failure

32. 1.Replace fluids…
 When the BGL reaches 300 mg/dL or less, the IV fluid may be changed
to D5W to prevent a precipitous decline in the BGL.
 Monitoring fluid volume status
 Vital Signs- orthostatic changes in BP and PR
 Lung assessment
 Intake and out put
 The calculated free water deficit (which averages 9–10 L) should be
reversed over the next 1–2 days (infusion rates of 200–300 mL/h of
hypotonic solution).
 In patients taking diuretics, the potassium deficit can
be quite large and may be accompanied by magnesium deficiency.
 Hypophosphatemia may occur during therapy and can be improved
by using KPO4 and beginning nutrition.

33. 2. Administer short-acting insulin:
 Regular Insulin 10units IV and 10 units IM, stat, then 0.1 units/kg
per hour by continuous IV infusion OR 5 units, I.V,boluses every
hour.
 If serum glucose does not fall by 50 to 70 mg/dL from the initial
value in the 2-3 hours, the insulin infusion rate should be doubled
every hour until a steady decline in serum glucose is achieved
Acidosis is reversed with insulin to inhibit fat break down, there by
stopping acid build up

34. Cont…
3. Potassium- All patients with DKA have potassium depletion
irrespective of the serum K+ level.
- If the initial serum K+ is <3.3 mmol/L ,do not administer insulin
until the K+ is corrected.
- If the initial serum K + is >5.3 mmol/L, do not supplement K+ until
the level comes to < 5.3.
- If K+ determination is not possible doelay intiation of K+
replacement until there is a reasonable urine put(>50 ml/hr)
- The serum potassium should be maintained between 4.0 and 5.0
meq/l
Add 40–60 meq/l of IV fluid when serum K+< 3.7 meq/L
Add 20- 40meq/l of IV fluid when serum K+ < 3.8 -5.2 meq/l

35. Cont…
4.Precipitant identification and treatment -noncompliance,
infection, trauma, infarction.
Initiate appropriate workup for precipitating event (cultures,
CXR, ECG)
5. Follow up of response- Blood glucose every 1–2 h, Urine
ketones every 4hr,electrolytes (especially K+) every 6 h for first
24 h.
6. Continuation of treatment – the above treatment should
continue until the patient is stable, ketone free.
7. Transition- Insulin infusion may be decreased to 0.05–0.1
units/kg per hour or 2-3 units,IV, hourly.
 Overlap in insulin infusion and SC insulin injection for about 3 -
5hr
8. SC long acting Insulin – start SC NPH as soon as the patient
eats. Monitor bloog glucose evry 4- 6 hour and give correctional
doses of regular insulin when needed.

36. Cont…
 When the patient is completely out of ketoacidosis, regular insulin is
given 4 hourly subcutaneously according to the random blood sugar
(RBG) level as follows:
 If RBG > 250mg/dl 12 Units
 If RBG - 180-250mg/dl 8 Units
 If RBG - 120-180mg/dl 4 Units
 IV fluid solutions with higher concentrations of glucose such as D5NS
or (D50, 0.45NS) are administered when BGLs reach 250-300 mg/dL
to avoid too rapid a drop in the BGL
 RBG < 120 mg/dl

37. Cont…
 Insulin must be infused continuously until subcutaneous
administration of insulin resumes
 BGLs are usually corrected before acidosis is corrected.
 Thus, IV insulin may be continued for 12-24 hrs until the serum
HCO3- level improves to at least 15 to 18 mEq/L and until the
patient can eat
NURSING ALERT
 Bicarbonate should be avoided, because of precipitation of sudden
hypokalemia

38. DKA: Nursing Management
 Monitoring fluid and electrolyte status, BGLs, ECG, V/S, ABGs
and other clinical findings
 Administering fluids, insulin
 Prevent other complications such as fluid over load
 As DKA resolved and potassium replacement rate is decreased, the
nurse makes sure that:
 There are no signs of hyperkalemia on the electrocardiogram (tall,
peaked or tented T-waves)
 The laboratory, values of potassium are normal or low
 The patient is urinating (i.e. no renal shut down)
 As the patient recovers, the nurse reassess the factors that may
have led to DKA and teach the patient and family

39. HHNS
 Is a metabolic disorder of T2D resulting from a relative effective
insulin deficiency (i.e., Insulin resistance) initiated by an inter-
current illness that raises the demand for insulin, associated with
polyuria and sever dehydration.
 Occurs most often in older people (50 to 70 years of age) who
have no known history of diabetes or who have type 2 diabetes

40. Cont…
 Nursing Management of Patients with DM
 Assessment
 Care Plan
 Nursing Diagnoses with interventions
1. Fluid Volume deficient may be related to, osmotic diuresis,
excessive gastric losses: diarrhea, vomiting, or restricted intake:
nausea, confusion, evidenced by weakness; thirst; sudden weight
loss, dry skin/mucous membranes, poor skin turgor, hypotension,
tachycardia, or delayed capillary refill

41. Cont…
 Nursing intervention: FVD
 Monitor vital signs:
 Monitoring
 Acetone breath
 Skin color/moisture, skin turgor, mucous membranes
 Capillary refill
 I&O; note urine specific gravity
 Weigh daily

42. Nursing intervention: FVD
 Administer fluids as indicate
 Insert/maintain indwelling urinary catheter.
 Monitor laboratory studies,
 Administer potassium and other electrolytes via IV and/or by oral
route as indicated.
 Insert NG tube and attach to suction as indicated

43. Cont…
 Imbalanced Nutrition, less than body requirements may be
related to, insulin deficiency, decreased oral intake: anorexia,
nausea, gastric fullness, abdominal pain; altered consciousness,
hypermetabolic state: release of stress hormones (e.g.,
epinephrine, cortisol, and growth hormone), infectious process
evidenced by increased urinary output, dilute urine; reported
inadequate food intake, lack of interest in food; recent weight
loss; weakness, fatigue, poor muscle tone; diarrhea; increased
ketones.

44. Nursing interventions
 Weigh daily or as indicated.
 Ascertain patient’s dietary program and usual pattern; compare
with recent intake.
 Auscultate bowel sounds. Note reports of abdominal
pain/bloating, nausea, vomiting of undigested food.
 Provide liquids containing nutrients and electrolytes as soon as
patient can tolerate oral fluids; progress to more solid food as
tolerated.
 Identify food preferences, including ethnic/cultural needs.
 Include so in meal planning as indicated.
 Observe for signs of hypoglycemia

45. Cont…
 Monitor laboratory studies, e.g., serum glucose, acetone, pH,
HCO3.
 Administer regular insulin by intermittent or continuous IV
method
 Administer glucose solutions, e.g., dextrose and half-normal
saline.
 Consult with dietitian for initiation of resumption of oral intake.
 Provide diet of approximately 60% carbohydrates, 20% proteins,
20% fats in designated number of meals/snacks

46. Cont…
 Risk for infection related to high glucose levels, decreased
leukocyte function, alterations in circulation; preexisting
respiratory infection, or UTI.
 Nursing interventions
 Observe for signs of infection and inflammation, e.g., Fever,
flushed appearance, wound drainage, purulent sputum, cloudy
urine.
 Promote good hand washing by staff and patient.
 Maintain aseptic technique for procedure
 Provide catheter/perineal care. Teach the female patient to
clean from front to back after elimination.

47. Cont…
 Provide conscientious skin care
 Auscultate breath sounds.
 Place in semi-fowler’s position.
 Reposition and encourage coughing/deep breathing
 Provide tissues and trash bag in a convenient location for sputum
and other secretions
 Encourage/assist with oral hygiene.
 Encourage adequate dietary and fluid intake
 Administer antibiotics as appropriate

48. Long term complications of DM

49. Diabetes mellitus: Complications
 Diabetes-related complications usually do not appear until the
second decade of hyperglycemia.
 Because type 2 diabetes mellitus (DM) often has a long
asymptomatic period of hyperglycemia before diagnosis, many
individuals with type 2 DM have complications at the time of
diagnosis.
 Fortunately, many of the diabetes-related complications can be
prevented or delayed with early detection, aggressive glycemic
control, and efforts to minimize the risks of complications.

50. Cont…
Diabetes-related complications can be divided into
vascular and nonvascular complications and are similar
for type 1 and type 2 DM
Nonvascular complications include gastroparesis,
infections, skin changes, and hearing loss.
The vascular complications of DM are further subdivided
into microvascular (retinopathy, neuropathy, nephropathy)
macrovascular complications (coronary heart disease
[CHD], peripheral arterial disease [PAD], cerebrovascular
disease).

51. GLYCEMIC CONTROLAND COMPLICATIONS
 The microvascular complications of both type 1 and type 2 DM
result from chronic hyperglycemia
 Evidence implicating a causative role for chronic hyperglycemia
in the development of macrovascular complications is less
conclusive.
 CHD events and mortality rate are two to four times greater in
patients with type 2 DM and correlate with fasting and
postprandial plasma glucose levels as well the

52. Cont…
 The general categories of long-term diabetic complications:
A. Macrovascular disease
B. Microvascular disease, and
C. Neuropathy
 The specific causes and pathogenesis of each type of complication
are still being investigated

53. Cont…
 Macro Vascular Complications (Macroangopathy)
 Can be seen both in diabetic and non-diabetic patients
 Result from changes in the medium to large blood vessels
 Blood vessels walls thicken sclerose and become occluded by
plaque that adheres to the vessel walls, and eventually blood flow
is blocked.

54. Cont…
 Blood vessel walls thicken, scleroses
 Occlusion by plaque that adheres to the vessel walls
 Blood flow is blocked
 Coronary artery disease Cerebrovascular disease
 Peripheral vascular disease
 Diminished peripheral pulses
 Intermittent claudication (pain in the buttock, thigh, or calf during
walking
 GANGRENE AMPUTATION

55. Micro Vascular Complications
 Are unique to diabetes
 Two areas affected:
A. Retina resulting in diabetic retinopathy
B. Kidneys resulting in diabetic nephropathy
 Retinopathy Occurs because of changes in the microvasculature:
 microaneurysms,
 intraretinal hemorrhage,
 Focal capillary closure

56. Cont…
 Retinopathy has three main stages:
 Nonproliferative (background),
 Preproliferative, and
 Proliferative widespread vascular changes (proliferation of new
blood vessels growing from the retina into the vitreous) and loss
of nerve fibers