Complications of Diabetes Mellitus & its Management.ppt

In diabetes mellitus (DM), years of poorly controlled hyperglycemia lead to multiple, primarily vascular, complications that affect small vessels (microvascular), large vessels (macrovascular) or both.

Immune dysfunction is another major complication and develops from the direct effects of hyperglycemia on cellular immunity.

1. Prof.Saranya.R,M.sc(N),[Ph.D],
Associate Dean
DhanalakshmiSrinivasan University
COMPLICATIONS OF
DIABETES MELLITUS

2. Objectives
•The Student will be able to
•list out the acute and chronic complications
•enumerate the etiology
•explain the pathophysiology
•discuss the clinical manifestations
•describe the collaborative management
•explain the nursing management

3. Introduction
Indiabetes mellitus(DM), years of poorly controlled hyperglycemia
lead to multiple, primarily vascular, complications that affect small
vessels (microvascular), large vessels (macrovascular) or both.
Immune dysfunction is another major complication and develops
from the direct effects of hyperglycemia on cellular immunity.

4. Acute complications of DM
Hypoglycemia
Diabetic Ketoacidosis
Hyperglycemic Hyperosmolar Non Ketotic Coma

5. •High bloodsugar
•DKA
•Dawnphenomenon:
Rise in blood sugar between 4 am and 8am
•Not associated with hypoglycemia(associatedwith diabetes type 1
and2)
•Somogyieffect -combination of hypoglycemia during night witha
rebound morning hyperglycemia that may leadto insulin resistance
for 12 to 48hours
HYPERGLYCEMIA

6. Serum glucose level < 55 mg/100ml
Brain damage develops when the brain is deprived of needed
glucose after a dramatic drop in blood sugar
insulin reaction, insulin shock, “the lows”
Mismatch between insulin dose, carbohydrate availability and
exercise
HYPOGLYCEMIA

7. CAUSES
Excess or overdose of insulin or OHA (oral hypoglycemic agents)
Skip meal or omitting a meal
Overexertion/ stress
Under-eating
Eating late
Unplanned exercise

8. HYPOGLYCEMIA-SIGNS &SYMPTOMS
MILD
Diaphoresis
Pallor
Paresthesia
Palpitations
Tremors
Anxiety

9. MODERATE
Confusion/ disorientation
Behavioral Changes
Cold clammy
extremities
Yawning
Tremors
Blurred vision
SEVERE
Seizures
Loss of Consciousness
Shallow respirations
Severe hypoglycemia can result in
death
Hypoglycemia -signs &symptoms

10. MANAGEMENT OF HYPOGLYCEMIA

11. RULES TOREMEMBER
Do not add sugar
RecheckFBS/CBG q 15 min
Avoid high fat (slows absorption of glucose)
Instruct: carry fast sugarlike lemon juice with sugar
Ifmeal is >1 hr away, complex carbohydratecan be given
NPO if “unconscious” or confused

12. Rules t oremember (contd)
15/15 rule: wait 15 minutes and monitor blood glucose; if still low
(BG<80), client should eat another 15 gm of sugar
Continue until blood glucose level has returned to normal
Client should contact medical care provider if
hypoglycemia occurs more than 2 or 3 times per week

13. HYPOGLYCEMIA TREATMENT -
UNCONSCIOUS
Glucagon 1 mgS/C, IM, IV; follow with oral or intravenous
carbohydrate raises blood sugar levels
Onset:10 minutes
Duration 25 minutes
subcutaneous / intravenous
Position: side lying
O r give 25mL of D 50 as IV push
followed by infusion of 5% dextrose in saline

14. Encourage to wear ID bracelet
Teach family that bevigilant insign of hypoglycemia
Carry simple sugar at all times
S&S or hypoglycemia
How to prevent Hypoglycemia
Check F B S if you suspect
HYPOGLYCEMIA-NURSING MEASURES

15. Serious complication of hyperglycemia due to lack of insulin
Usually occurs with type I DM(> 250mg/dl)
Results from breakdown of fat and overproduction of ketones by
the liver and loss of bicarbonate
DKA(Diabetic ketoacidosis)

16. •Cause: illness, infection, stress (physical or emotional stress)
•Surgery, trauma, pregnancy
•Absence or inadequate insulin
•-Taking too little insulin
•-Omitting doses of insulin
•Known diabetic has increased energy needs
•Initial or undiagnosed diabetes
•Developing insulin resistance
DKA–ETIOLOGY

17. Hyperglycemia
Dehydration
Electrolyteloss
MetabolicAcidosis
DKA-MAIN CLINICALFEATURES

18. PATHOPHYSIOLOGY -DKA
NoInsulin
Glucose stays in
blood -
Hyperglycemia
Muscle not
getting energy
High fat
metabolism
Osmoticdiuresis
Polyuria
Polydipsia
Electrolyteloss
Increased ketone in
blood
MetabolicAcidosis
i ncreaseserum
pH
Dehydration
h ighespiratoryrate

19. Environment, infection,
emotional stress
Lack ofinsulin
Breakdown of fats in
cells
Free fatty acids to
liver
Formation ofketone
bodies
Ketones inurine
andblood
Breakdown of
glycogen to
glucose
Decreased
use of
glucose
Protein
breakdown
Hyperglycemia
Osmoticdiuresis
Dehydration
Hyperosmolalityand
Hemoconcentration
Acidosis COMA
Gluconeo-
genesis
Increased
BUN
Electrolyte
imbalance

20. SIGNS AND SYMPTOMS O FDKA
Hyperglycemia-↑bloodglucose
Tired
Polyphagia
Decreased attention,confusion
N/V, abdominalpain
Blurredvision

21. SIGNS AND SYMPTOMS OFDKA
Dehydration
Polydipsia
Polyuria
Dry/flushedskin
Orthostatichypotension
Tachycardia
Headaches
Decreased Na+ and K+levels

22. Signs and symptoms of DKA
Acidosis
Resp. ratedecreased
Kussmaul’s
Fruity breath, acetonebreath
SerumpH
Decreased
Normal Serum pH 7.35 –7.45
pH = acidic /acidosis
pH = alkaline/alkalosis

23. •Blood
Serum Osmolalityhigh-Ketones present
Bicarbonateless than 15 mEq/L
Decreased K
+
levels pH less than 7.35.
•Sugar levels-Elevated greater than 250 mg/dL
•BUN Blood Urea Nitrogen -increased
•Dehydration
DKA:DIAGNOSIS

24. MANAGEMENT OFDKA
Focus on the four main clinicalfeatures
Hyperglycemia
Dehydration
Electrolyteloss
Acidosis

25. Hyperglycemia
Administer insulin IV
Dehydration
Rehydrate
IV, pushfluids
I&O
Check vitalsigns
Check Lungsounds
Monitor labvalues
MANAGEMENT OFDKA

26. MANAGEMENT OF DKA
Electrolyteloss
ReplaceK+
Monitor lab valuesclosely

27. HYPER OSMOLAR HYPERGLYCEMIC NON KETOTIC
COMA (HHNK)
Occurs when there is insufficient insulin to prevent hyperglycemia, but
there is enough insulin to prevent ketoacidosis
Occurs in all types of diabetes (esp diabetes type 2)
Life threatening medical emergency, high mortality rate
Characterized by Plasma osmolarity 340 mosm/L or greater (normal:
280 -300)
Blood glucose severely elevated, 600 –1000 or 2000 (normal 70-110)
Altered level of consciousness

28. Extreme hyperglycemia
(800-1000mg/dl)
Undetectable ketonuria
Absence of acidosis
Major difference from diabetic keto acidosis is the lack of
ketonuria because there is some residual ability to secrete insulin
in NIDDM.
HHNKS

29. Infection (mostcommon)
Therapeutic agent orprocedure
Acute or chronicillness
Overeating
Stress
Too littleinsulin
Precipitating factors

30. Renalinsufficiency
Severehyperosmolality
Intracellulardehydration
Hypovolemia
Shock
Tissuehypoxia
ExtracellularDehydration
COMA

31. •Altered level of consciousness (lethargy to coma)
•Neurological deficits: hyperthermia, motor and sensory
impairment, seizures
•Dehydration: dry skin and mucous membranes, extreme thirst
Signs And Symptoms Of HHNK Syndrome

32. Usually admitted to intensive care unit of hospital for care since
client is in life-threatening condition: unresponsive, may be on
ventilator, has nasogastric suction
vigorous fluid replacement
give insulin IV Lower glucose with regular insulin until glucose
level drops to 250 mg/Dl
potassium, sodium chloride given IV
dextrose is given when blood sugar reaches around
250mg/100ml to prevent hypoglycemia
Treat precipitating factors
MANAGEMENT

33. NURSINGRESPONSIBILITY
Same as withDKA
Insulin
Hydration
Electrolyte replacement andmonitoring
Treat underlyingcause

34. Macrovascular complications
Arteriosclerosis
Characterized by thickening and loss of elasticity of the arterial
walls “hardening of the arteries”.
Coronary Artery Disease
Cerebrovascular Disease
Peripheral vasculardisease
Micro vascular complications
Characterized by basement membrane thickening
Effects smallest blood vessels
Due to hyperglycemia
CHRONIC COMPLICATIONS

35. Major source of mortality in patients with type2 DM.
Approximately two thirds of people with diabetes die of heart disease or
stroke.
Men with diabetes face a 2-fold increased risk for chd, and women have
a 3-to 4-fold increased risk
Diabetics more likely to develop MI, congestive heart failure
Cardiovasculardisease

36. About two out of three people with diabetes die of heart diseasetwo to
four times higher risk for stroke.
ATHEROSCLEROSIS

37. •Affects 20 –60 % of all diabetics
•Increases risk for retinopathy, nephropathy
HYPERTENSION

38. Increased risk for Types 1 and 2 diabetics
Development of arterial occlusion and thrombosis
resulting in gangrene
Gangrene from diabetes most common cause of non-
traumatic lower limb amputation
PERIPHERAL VASCULAR DISEASE

39. Diabetes is the leading cause of kidney
failure, accounting for 44% of new
cases in 2008.
Most common cause of end-stage renal
failure in U.S
Glomerular changes in kidneys of
diabetics leading to impaired renal
function
DIABETICNEPHROPATHY

40. AKA -Kimmelstiel-Wilson syndrome
is a kidney condition associated with long-standing diabetes
glomerulosclerosis associated with diabetes
First indicator: microalbuminuria
DIABETICNEPHROPATHY

41. Diabeticswithouttreatmentgoontodevelophypertension,edema,
progressiverenalinsufficiency
In type 1 diabetics, 10 –15 years
May occur soon after diagnosis with type 2 diabetes since many are
undiagnosed for years
DIABETICNEPHROPATHY

42. Cont.. DIABETICNEPHROPATHY
Damage to the tiny blood vessels within the kidney.
Due to
Hyperglycemia
hi g h glucose levels
Stress kidney’s filtration mechanism
Blood protein leaks into urine
Pressure in blood vessel of kidney high
Kidney failure

43. Proteinuria / albuminuria
Reduce urine output
Edema
BUN & Creatinine ↑
SIGNS &SYMPTOMS

44. Tight glucose control
Anti-hypertensives
Calcium-channel blockers
Alpha blockers
ACE inhibitor
DialysisTransplant
PREVENTION
Control blood glucose
Control hypertension
Treat UTI
No nephrotoxic substances
Nephropathy: management & prevention

45. Definition:Diabetic Retinopathy refers to the process of damage to the
tiny blood vessels that supply the eye
Incidence:
Retinal changes related to diabetes
DMis the major cause of blindness in adults aged 20-74 years in US
accounts for 12,000-24,000 newly blind persons every year.
Affects almost all Type 1 diabetics after 20 years
Affects 60 % of Type 2 diabetics
DIABETICRETINOPATHY

46. •Classifications:
Non proliferative most common. Partial occulusionofblood vesseles
cause retina becausemicroaneurysmto develop in the capillary it leaks
the fluid and causes the retinal edema and exudates or intraretinal
hemorrhage.
Proliferative sever form it involves the retina and viterous. Retinal
capillaries become occuludedthe body compensate to make new blood
vesseles, a pathologic process called neovascularization, these
vessels are extremely fragile and hemorrhage easily, and hemorrhage
easily.newblood vessels pull retina and causing retinal detachment.
DIABETICRETINOPATHY

47. DIABETICRETINOPATHY

48. Control
Glucose
BP
No straining
Use laxatives
Avoid lowering head
Avoid lifting above shouldersDiabetics should be screened
for retinopathy
PREVENTION

49. •Management
good glycemic control
Managing Hypertension
Laser photocoagulation (destroy the ischemic area of retina)
Vitrectomy (aspiration of blood, membrane, and fibers from inside of
the eye through small incision just behind the cornea.
Vascular endotheleal growth factor drug injected into the eye that
block the action of reduce inflammation
RETINOPATHY

50. •Cataracts
•LensChanges
•Extraocular muscle palsy
•Glaucoma
OTHER OPTICCOMPLICATIONS

51. Diabetic Neuropathy

52. Definition:
It refers to nerve damage that occurs because of
metabolic dearrangement associated with diabetes mellitus.
Etiology:
•Metabolic
•Vascular
•Autoimmune factors
Diabetic Neuropathy

53. Signs and symptoms:
AKA peripheral neuropathy
Paresthesias: primarily lower extremities
decreased deep tendon reflexes
Numb feet
Decrease sensation
Unsteady gait
High risk foot injury
SENSORY-MOTORPOLYNEUROPATHY(stocking glove
neuropathy)

54. Autonomic NS
Can affect almost any system
Cardiovascular
Tachycardia
Orthostatic hypotension
MI
Gastro-intestinal
Delayed gastric emptying
Constipation
Diarrhea
Urinary
Retention
Neurogenic bladder
AUTONOMICNEUROPATHY

55. Reproductive
Maleimpotence
AdrenalGland
“HypoglycemicUnawareness”
AdrenalMedulla
Adrenergicsymptoms
No longer feelS&S
Strict BG control & frequentmonitoring
Sudomotorneuropathy
Nosweating
Anhydrosis
dryfeet
footulcers
AUTONOMICNEUROPATHY

56. •Control serum glucoselevels
•Paincontrol
Analgesics(non-narcotic)
Tri-cyclicantidepressants
Anticonvulsants
MANAGEMENT

57. DIABETES MELLITUS-INFECTIONS
Increased susceptibility toinfection
Predisposition is combined effect of other complications
Normal inflammatory response isdiminished
Slower than normalhealing
Periodontaldisease
Foot ulcers and infections: predisposition is combined effect of
othercomplications

58. High risk of foot infections
Neuropathy
•Pain sensation decrease
•Pressure sensation decrease
•Dryness
•Fissures
•Duration ofdiabetes
•Increasing age
•Smoking
•Decreased peripheral pulse
•Decreased sensation
•Deformity
•ulcers

59. FOOT INFECTIONS

60. MANAGEMENT OF INFECTIONS
•Bed rest
•Antibiotics
Topic vs. IV
•Debridement
•Control Glucose levels
•Amputation
•Teach foot care
Prevention
•Teach wound care

61. 1. Managingdiabetes
2. Lowering risk factors forconditions
3. Routine screening forcomplications
4. Implementing earlytreatment
PREVENTION OF COMPLICATIONS

62. NURSING MEASURES
•Interventions and foot care practices:
–Cleanse and inspect the feet daily.
–Wear properly fitting shoes.
–Avoid walking barefoot.
–Trim toenails properly.
–Report non healing breaks in the skin

63. References
•Lewis L. Kinkle2018 Text book of Medical and Surgical
Nursing Assessment and Management of Clinical Problems
2
nd
South Asian edition, Mosby, Elsevier publisher, Missouri.
•Brunner and Suddarth2000 Text book of Medical and
Surgical nursing 10
th
edn, Wolterkluwercompany ,London.
•Joyce M block 2009 Text book of Medical and Surgical
nursing,8
th
edn, Elsevier company UP
References

64. THANK YOU