Clinical Manifestations

The disease processes of type 1 diabetes mellitus (DM1) often precede the symptoms by several years, but the clinical manifestations of hyperglycemia usually include:

• Polyuria- excessive urination
• The amount of glucose filtered by the kidneys exceed the amount that can be reabsorbed. As a result, hyperglycemia leads to osmotic diuresis; glucose is lost in the urine along with with large amounts of water

• Polydipsia- increased thirst
• Elevated blood glucose levels cause fluid to be osmotically pulled out of tissues into the bloodstream and leads to intracellular dehydration and the stimulation of thirst by the hypothalamus

• Polyphagia-increased appetite
• Depletion of carbohydrates, fats, and protein stores results in cellular starvation and an increase in hunger

• Weight loss
• Occurs because of fluid loss, and fat and protein breakdown

• Fatigue
• Metabolic changes result in poor use of food products

• Sudden vision changes
• Occurs as fluid balance in eye fluctuates because of elevated blood glucose levels; see diabetic retinopathy below

• Parethesia- tingling or numbness in hands and/or feet
• The result of diabetic neuropathy

• Recurrent infections
• Diabetes is associated with some levels of immunodepression; increased blood glucose levels promote the growth of microorganisms, and impaired blood supply hinders wound healing

(Strayer & Schub, 2011; Huether et al., 2012, p.461)

Blood Glucose Measurement:

• As summarized by the American Diabetes Association, two systems are used to determine normal values of blood glucose. Either 3.6-5.8 (4-6 average) mmol/L = international units (used in Canada), or, 64.8-104.4 mg/dL (used in the U.S.). The International system uses molar concentration and the U.S. uses mass concentration. A quick way to navigate between the two systems, if necessary, is to either divide the American mass figure by 18, or multiply the International system of # moles by 18. The reason for this is that the molecular weight of glucose C6H12O6 is approximately 180 g/mol to 1 mmol/L of glucose is equivalent to 18 mg/dL (American Diabetes Association, 2010).

                                                                 Glucose-test
                                                                 
Diagnostic Criteria For Type 1 and Type 2 Diabetes Mellitus  
1. Glycosylated hemoglobin, HbA_1c (as measured in a Diabetes Control and Complications Trial-reference assay) > 6.5 % (Huether et al., 2012, p.459)
                                                     OR

2. Fasting plasma glucose (FPG) level > 126 mg/dl or 7.0 mmol/L (Canadian Diabetes Association, 2008)     
                                                     OR

3. 2-hr (non-fasting) plasma glucose level > 200mg/dl or 11.1mmol/L during a 75g oral glucose tolerance test (Canadian Diabetes Association, 2008)
                                                     OR

4. Symptoms of hyperglycemia, a 2 hour plasma levels during at oral glucose tolerance test (OGGT) plasma glucose > 200mg/dl or 11.1mmol/L (Canadian Diabetes Association, 2008)

• FPG is defined as no caloric intake for at least eight hours.

• Glycosylated hemoglobin Hb_Ac1- the percentage of glucose attached permanently to hemoglobin molecules; a measure of average plasma glucose exposure over the life span of the RBC (120 days).

• In the absence of hyperglycemic symptoms, criteria 1-3 should be repeated to confirm results.

(Huether et al., 2012, p.460)

• Casual is defined as anytime during the day without any regard to meals (Canadian Diabetes Association, 2008)

 
Differentiating Type 1 DM from Type 2 DM

• Islet cell auto-antibodies
• Present in early-stage DM1, but absent in DM2

• C- peptide,
  
  • A component of proinsulin released during insulin production
  • Indicative of beta-cell function and insulin production
    
  • Levels are decreased in DM1 and normal or elevated in DM2

(Ballard, 2009)

• Type 1 Diabetics experience hypoglycemia more often than type 2 diabetics, 43/person/year versus DM2 at 16/person/year (Briscoe & Davis, 2006). (http://clinical.diabetesjournals.org/content/24/3/115.full)

• Diabetic ketoacidosis is a cardinal symptom (Welch & Zib, 2004) of DM1
  • It is thought to never occur in DM2 but does occasionally (http://clinical.diabetesjournals.org/content/22/4/198.full)

• Type 1 Diabetics are more at risk for osteoporosis than DM2 (Simon, 2009)
  

Common Acute Complications:

Hyperglycemia: The symptoms of acute hyperglycemia are the same as those found above in the initial signs and symptoms that first indicate an individual has diabetes: non-fasting blood glucose above 7- 8 mmol/L, polyuria, polydipsia and polyphagia, blurred vision, dry mouth, stupor and in very high blood glucose levels, possible seizures or coma.
 

Hypoglycemia (insulin shock/reaction)

• A low plasma glucose level < 4.0 mmol/L (Canadian Diabetes Association, 2008)
  
• Individuals with type 1 diabetes are more at risk for hypoglycemia
• Adrenergic symptoms: pallor, sweating, tachycardia, palpitations, hunger, restlessness, anxiety, and tremors
  
• Neurogenic symptoms: fatigue, irritability, headache, loss of concentration, visual disturbances, dizziness, confusion, transient sensory or motor defects, convulsions, coma and death
  
• Rapid onset
• Risk factors
  • Excessive insulin or sulfonylurea agent intake
  • Insufficient food intake
  • Excessive physical activity
  • Excessive alcohol consumption
    
  • Abrupt decline in insulin needs e.g. renal failure
    
  • Simultaneous use of insulin-potentiating agents or beta-blocking agents that mask symptoms (Huether et al., 2012, p. 464)  

Diabetic Ketoacidosis (Diabetic coma syndrome)

• The increased metabolism of fats and proteins contributes to hyperglycemia and the build-up of ketones in the body. The accumulation of ketone bodies causes pH to drop, resulting in metabolic acidosis
• Diagnostic Criteria
  • Blood glucose level >250 mg/dl or 13.9 mmol/L
  • Venous pH <7.3
  • Serum bicarbonate <15.0 mmol/L (Ballard, 2009)
  • Presence of an anion gap
  • Presence of urine and serum ketones
• Symptoms include
  
  • Fruity or acetone odour on the breath
  • Kussmaul respirations/hyperventilation
    
  • Altered level of consciousness
  • Abdominal pain
  • Nausea and vomiting
• Slow onset
  
• Risk factors
  
  • Stressful situations e.g. infection, accident, trauma, emotional stress
    
  • Very low levels of insulin
    
  • Medications that antagonize insulin (Huether et al., 2012, p.464; Strayer & Schub, 2011)

Chronic Complications

Microvascular

• Retinopathy
  • The most common cause of new cases of legal blindness is diabetic retinopathy (Canadian Diabetic Association, 2008)

• Three Stages (Huether et al., 2012,p.467)
  • Nonproliferative- characterized by increased retinal capillary permeability, vein dilation; micro-aneurysms and hemorrhaging occur as a result of weakened blood vessels
    
    • May be asymptomatic
  • Preproliferative- as the condition progresses, blood vessels can become blocked and blood supply is cut off (Simon, 2009)
    
  • Proliferative- new abnormal blood vessels and fibrous tissue are formed within the retina or optic disc; as a result, retinal detachment and vitreal hemorrhaging may occur
    
    • Can lead to loss of visual acuity or blindness
• Macular edema can occur at any stage of diabetic retinopathy; Fluid enters the macula causing it to swell, leading to the loss of central vision and blurred vision (Simon, 2009)

• Nephropathy
  • Kidney damage leads to the presence of proteins in the urine
    
  • Microalbuminuria-small amounts of albumin in the urine
    
    • First sign of kidney dysfunction
  • Continuous proteinuria carries a life sentence of less than 10 years
  • Hypertension gradually leads to end-stage kidney failure

(Huether et al., 2012, p.467 )

• Prevention (Simon, 2009)
  
  • maintain Hb_A1c level at < 7%
  • Control blood pressure
  • Lower LDL cholersterol and triglycerides levels

• Neuropathy
  • Risk factors include hyperglycemia, elevated triglycerides, high body mass index, smoking and hypertension (Simon, 2009)

• Peripheral neuropathy
  • Affects the toes, feet, leg, arms and hands (Simon, 2009)
    
  • Symptoms:
    
    • Loss of sensation and motor nerve function,small muscle atrophy, weakness, tingling and numbness
      
    • Acute painful peripheral neuropathy with deep, burning pain in legs and feet can also occur (Huether et al., 2012,p.466)
      

• Autonomic neuropathy
  • Affects the heart and blood vessels, digestive system, urinary tract, sex organs, sweat glands, eyes and lungs (Simon, 2009)
• Expressed as visceral manifestations that include:
  
  • Delayed gastric emptying, diarrhea, altered bladder function, erectile dysfunction and impotence, postural hypotension, and changes in heart rate (Huether et al., 2012, p.466)

• Skin and foot lesions
  • Peripheral neuropathy, poor circulation and suppressed immunity put diabetics at risk for:
    
    • pressure ulcers and delayed wound healing
    • abscess formation
      
    • development of necrosis and gangrene
    • infection
      
    • osteomyelitis-bone infection
      
    • amputation

(Huether et al., 2012, p.466)

Macrovascular 

• Cardiovascular complications:
  • Atherosclerosis
    • The hardening of arteries due to build up of fatty deposits
      
    • Can lead to coronary artery disease, heart attack and stroke
  • Hypertension
    • Occurs if kidneys are damaged
    • Can lead to heart attack, stroke, and heart failure
  • Cardiomyopathy
  • Heart failure

(Huether et al., 2012,p.466; Simon, 2009) 

• Cerebrovascular complications:
  
  • Ischemic and thrombotic stroke
    • risk factors include hypertension, hyperglycemia, hyperlipidemia and thrombosis

• Peripheral vascular disease
  
  • Most gangrene that occurs in the lower extremities are caused by occluded arteries and arterioles
  • Ulcers can worsen into osteomyelitis or gangrene requiring amputation

(Huether et al., 2012, p.466-468)

 
Infection

• Diabetics are at greater risk for developing respiratory,wound and urinary tract infections, as well as sepsis (Huether et al., 2012,p.466-68; Simon, 2009)

Psycho-social Factors

Diabetics face a daily, sometimes hourly task of monitoring the work of a dysfunctional organ. A diabetic child's family and diabetics themselves have to be vigilant about their tasks, unlike many other diseases. Unlike non-diabetics, the consequences of not being focused everyday on the burden of blood sugar readings and insulin medications can have very significant and critical results. It is not surprising that psychological and social issues are a large part of the disease and need to be addressed:

• Depression, anxiety, eating disorders, behavioural problems, family conflict and maternal distress can be issues in children with DM1.
• Clinical depression and subclinical levels of mood disruption, anxiety and eating disorders are associated with adults with DM1.

Several studies have shown that youth with DM1 are at a greater risk for developing anxiety disorders, eating disorders, and adjustment disorders. Children with such chronic illnesses are prone to worrying about shortened life expectancy, interference with schooling, career choices, and leisure activities (Kanner, Hamrin & Grey, 2003).

Research shows that depression and quality of life is greater in adults with more microvascular and macrovascular complications and that increased control of blood glucose regulation leads to a remission of depression. Statistics have indicated that diabetic depression affects suicide and suicidal ideation by a tenfold increase (Kanner, Hamrin & Grey, 2003). Also, depression lessened with intervention, even when the overall changes towards blood glucose control, were not very significant. This suggests that special supportive intervention programs that include regular assessment for both diabetic children and their families and adult diabetics is very important.

Nursing treatment for depression is classified as either pharmacologic, psychosocial, or the combination of the two. With diabetic patients, efforts must be made to intervene by psychosocial methods first. Some of the items in the assessment tools of nurses are the family, academic, social and psychiatric situation of the patient. Nurses can educate the patient and family about diabetes and treatment options. This time period will also allow the nurse to build a therapeutic relationship with the patient (Kanner, Hamrin & Grey, 2003).