MedSurg Exam 3

Continuum of Thyroid Dysfunction

Thyrotoxicosis ← Hyperthyroidism ← Euthyroid → Hypothyroidism → Myxedema Coma

Hyperthyroidism ←        Metabolism                      →Hypothyroidism

Hyperthyroidism

FAST FAST

• A sustained increase in synthesis and release of thyroid hormones by thyroid gland (hyperactivity of glands)

• Occurs more often in women

• Highest frequency between ages 20 to 40 years

• The most common form is Graves disease. Other causes include toxic nodular goiter, thyroiditis, excess iodine intake, pituitary tumors, and thyroid cancer 

• Exhibited by:

  • High T₄ and T₃: can be normal for subclinical 

    • Results in low TSH

Hyperthyroidism diagnosis

• RadioActive Iodine Uptake Test/RAI-U: 

  • Measures how much radioactive iodine your thyroid absorbs from your bloodstream:

    • Iodine is used by your thyroid to make hormones

  • Helps differentiate different causes of hyperthyroidism:

    • Graves Disease:

      • High uptake of iodine: uptake of 90%

        • Autoimmune disease which causes overproduction of thyroid hormone

Hyperthyroidism etiology 

• Most common:

  • Graves’ disease

• Other:

  • Toxic nodular goiter

  • Thyroiditis (inflammation of thyroid gland) = can be viral or bacterial infection, subacute/acute have abrupt onset with reports of thyroid pain/radiating pain in surrounding areas 

- Manifestations = fever, chills, sweats, and fatigue 

• Excess iodine intake

• Tumor 

Hyperthyroidism main manifestations

• Thyrotoxicosis

• Goiter

• Exophthalmos

Hyperthyroidism systemic manifestations

• Cardiovascular Issues: FAST FAST 

  • Systolic HTN

  • Bounding, rapid pulse; palpitations

  • Increased CO

  • Ventricular hypertrophy

  • Systolic murmurs

  • Dysrhythmias

  • Angina

• Respiratory System: What comes with fast HR and chest pain? 

  • Dyspnea on mild exertion

  • Tachypnea

• GI System: REMEMBER HYPERMETABOLISM 

  • Increased appetite and thirst

  • Weight loss:

    • Increased metabolic rate

  • Diarrhea

  • Splenomegaly

  • Hepatomegaly

• Skin: 

  • Diaphoresis:

    • Warm, smooth, moist skin

  • Thin, brittle nails

  • Hair loss

  • Clubbing of fingers (acropachy) 

  • Palmar erythema:

    • Redness or flushing of the palms of the hands

    • Fine, silky hair:

      • Premature graying in men

    • Vitiligo 

    • Intolerance to heat

    
    

    • MSK:

      • Fatigue

      • Weakness

      • Proximal muscle wasting

      • Dependent edema

      • Osteoporosis 

    
    

    • NS:

      • Hyperactive deep tendon reflexes

      • Nervousness

      • Fine tremors

      • Insomnia

      • Difficulty focusing eyes

      • Lability of mood:

        • Rapid fluctuations in mood

      • Delirium/agitated -> may be confused with dementia delaying diagnosis  

      • Lack of ability to concentrate

      • Stupor

      • Coma

      • Intolerance to rapid speech

      • Hyperreflexia 

    
    

    • Reproductive:

      • Menstrual irregularities

      • Amenorrhea

      • Decreased libido and fertility

      • Impotence and gynecomastia (boobies) in men

Thyrotoxicosis

• Excessive thyroid hormone leads to hypermetabolism:

  • Physiologic effects/clinical syndrome of hypermetabolism

• Results from increased circulating levels of T₃, T₄ or both

• Hyperthyroidism and thyrotoxicosis usually occur together

Goiter

• Enlargement of the thyroid gland 

• Common cause is lack of diet iodine 

• Other causes = overproduction/underproduction of thyroid hormones, Goitrogens (food containing thyroid-inhibiting substances) 

• Nontoxic = enlarged thyroid with normal thyroid hormones levels

• Nodular = thyroid hormone-secreting nodules that makes it lumpy

• Toxic = causes hyperthyroidism, found in graves disease → enlargement

• Palpate to feel enlargement

• Auscultation:

  • Bruits (blood supply also has gotten larger), not related to carotid arteries. 

• Measure TSH, T4 levels, thyroid antibodies (thyroiditis)

• Treatment involves thyroid hormone or surgery  

Exophthalmos

• usually Bilateral, classic sign 

  • Increased fat deposits and fluids around the eye, edema: Issue of cornea and upper eyelids

    • Eyeballs are forced outward due to increased pressure:

      • Eyes get very dry: 

        • Provide eye drops and tape eyelids close

• Corneal ulcers and loss of vision, plus diplopia (see two images of an object)

• Test with 6-cardinal gaze 

Etiology and Pathophysiology of Graves’ Disease

• Pt develops antibodies to TSH receptors:

  • Stimulates thyroid (over produce) to release more T₃ and T₄ 

• Autoimmune disease: Antibodies to T hormones -> high T3/4 production

  • Diffuse/Uniform thyroid enlargement

  • Excess thyroid hormone

• Causative factors interact with genetic factors:

  • Smoking

  • Infection

  • Stress

  • Lack of Iodine in diet:

    • Exacerbates hyperthyroidism:

      • Iodized salt prevents this

• Women are 5 times more likely than men to develop Graves’ disease

Graves’ Disease onset and complications

• Has remissions and exacerbations: 

  • Leads to destruction of thyroid tissue which leads to hypothyroidism

  • Not always showing signs and symptoms of condition

• Might be seen with other autoimmune diseases like:

  • Rheumatoid Arthritis (RA)

  • Systemic Lupus Erythematosus (SLS)

  • Celiac’s Disease

  • Addisons’s Disease

Complications (life threatening)

• Acute thyrotoxicosis (thyroid storm) due to infection, trauma, surgery 

• Manifestations include tachy, Hr, shock, hyperthermia, agitation, delirium, seizures, abdominal pain, vomiting, diarrhea, and coma 

• If there is a crisis, the cardio and respiratory will not be able to keep up 

• Patients who are getting their thyroid removed are at risk as the tissue is manipulated and thyroid gland release all their hormones at once 

• Can result in death if not treated 

Hyperthyroidism interprofessional care

• Diagnostic studies = TSH (<0.4 mU/L), T3/4 levels + RAIU test to distinguish graves disease from other forms of thyroiditis (graves will have uptake of 35-95%) 

3 Primary Treatment Options:

• Antithyroid Medications

• RadioActive Iodine Therapy

• Surgery: Usually take part, not whole thyroid gland expect cancer

• Nutrition

Antithyroid Medications

• not curative but help control symptoms 

  • Useful in the treatment of thyrotoxic states, but it is not curative:

    • Antithyroid medications:

      • Propylthiouracil: rapid reduction in symptoms (3x a day)  

      • Methimazole (common): 1x a day 

        • See improvement in 2 weeks

        • Continued for 6-15 months for spontaneous remission but adhere to meds or return of hyperthyroidism  

        • No curative just controlling symptoms

SURGERY  

• Iodine = prepare pt for thyroidectomy or treatment of thyrotoxicosis (effect within 1-2 weeks, not longterm) 

- Toxicity = swelling of buccal mucosa, excess salivation, nausea, vomit, and skin reactions 

• Beta Adrenergic blockers: Atenolol/Propranolol 

  • Prevents tachycardia and dysrhythmias

RadioActive Iodine Therapy

• You prego this not for you 

  • Treatment of choice for non-pregnant patients

  • Damages or destroys thyroid tissue:

    • Delayed response of up to 3 months so patients take antithyroid drugs and propranolol during the 3 months for RAI to take effect 

    • May need posttreatment hypothyroidism for life 

    • Radiation thyroiditis, parotitis, dryness, and irritation of mouth/throat so drink water, ice chips/salt with soda, etc 

    • Teach RAI precautions like using private toilet facilities,flush 2-3 times after each use, not preparing food that need prolonged exposure using bare hands, and avoid being close to pregnant/children for 7 days after therapy     

Hyperthyroidism Surgery

• Usually take part, not whole thyroid gland expect cancer 

• Antithyroid drugs, iodine, and B-adrenergic blockers may be given to achieve a euthyroid state before surgery  

  • Airway preservation is the best indication to do surgery

  • There will be rapid reduction in T₃ and T₄ levels:

    • Leads to hypothyroidism

  • Preference is to do subtotal thyroidectomy where about 90% of thyroid is removed

  • Invasive endoscopic (<3 cm, no cancer) or robotic thyroidectomy (overweight, small nodules on 1 side) 

  • Increased risk for thyrotoxicosis

  • Post-Op Care:

    • Monitor for:

      • Swelling/obstruction of airway:

        • Biggest concern if observed after thyroidectomy 

      • RR

      • Breathing

      • SaO₂

    • Have trach + O2 suction set ready in bedside

    • Monitor for complications:

      • HR, dysrhythmia  

      • Hypothyroidism + thyroid storm

      • Parathyroid loss or damage → Hypocalcemia:

        • PTH can be damaged: Tetany 

          • Trousseau

          • Chvostek

•  IV Ca⁺ available at the bedside

• Hemorrhage

• Laryngeal nerve damage → laryngeal stridor 

• Thyrotoxicosis

• Infection

• Body image = reassure patient the scar will fade in color and look like a normal neck wrinkle 

Nutrition for hyperthyroidism

• High calories diet (4000-5000 cal/day) -> 6 full meals with high protein,carb, vitamins, and minerals snacks

• Protein should be 1-2 g/kg of ideal body weight 

• Avoid highly seasons and high fiber foods, plus caffeine containing liquids -> low salt due to edema 

• Goals:

  • Block adverse effects of thyroid hormones

  • Suppress hormone oversecretion

  • Prevent complications

Acute Thyrotoxicosis/Thyroid Storm

• Excessive amounts of hormone released

• Life-threatening emergency

• Death rare when treatment started early

• Results from stressors

• Thyroidectomy patients at risk:

  • Can cause more hormones to be released 

Acute Thyrotoxicosis/Thyroid Storm manifestations 

• Extreme metabolic demand:

  • Severe tachycardia;

    • Leads to HF:

      • Shock

  • Hyperthermia:

    • Up to 106°F/41.1°C

• Agitation

• Seizures

• Abdominal pain

• Vomiting

• Diarrhea

• Delirium

• Coma

Acute Thyrotoxicosis/Thyroid Storm implementation

• Necessitates aggressive treatment

• Give medications that block thyroid hormone production and SNS effects

• Monitor for dysrhythmias

• Ensure adequate oxygenation

• Fluid and electrolyte replacement

• If exophthalmos present:

  • Apply artificial tears to relieve eye discomfort

  • Restrict salt and elevate head of bed:

    • Iodized salt has iodine in it

  • Dark glasses

  • Tape eyelids close if needed for sleep

  • ROM of intraocular muscles

Hypothyroidism

slow slow 

• More common

• Deficiency of thyroid hormone

• Causes general slowing of metabolic rate

• More common in women than in men

• Subclinical will have TSH greater than 4.5 mU/L and T4 normal while overt have increased TSH and decreased T4 levels 

• Nonthyroidal illness syndrome (NTIS) = low T3/4, and TSH levels  → no h/x or current thyroid dysfunction

Hypothyroidism etio

• Iodine deficiency: iodine salt (helped to prevent iodine deficiency) 

  • Most common

• Atrophy of the gland:

  • Common in the US:

    • Hashimoto’s thyroiditis (HT, destruction of thyroid tissue by antibodies)

- Goiter is hallmark sign (changing voice, affect breathing)

- Transient phase of hyperthyroidism due to leaking thyroid hormone from damaged tissues 

- Silent, painless thyroiditis = early HT in postpartum women 

- T3/4 are low while TSH level is high 

- Treatment = Antibiotics, surgical drainage, NSAIDs (subacute/acute), corticosteroids (severe pain), propranolol/atenolol

- Teach patients to stay on meds, any change in symptoms, plus patients are risk of Addison disease, pernicious anemia, or graves disease

• Graves’ disease:

  • Thyroid overactive:

    • Gives up

• Treatment for hyperthyroidism like surgery or RAI therapy 

• Drugs like amiodarone 

• Cretinism if occurs in infancy

Hypothyroidism patho

• Types:

• Primary:

  • Caused by destruction of thyroid tissue or defective hormone synthesis

  • Atrophy of thyroid gland from HT or graves (common) 

• Secondary:

  • Caused by pituitary disease (decreased TSH)

  • hypothalamic dysfunction (decreased TRH):

    • Fix pituitary to cure

Hypothyroidism manifestations

• Systemic effects are characterized by slowing of body processes

• Manifestations variable 

• Slow onset: Patient does not recognize the signs while using other excuses like im getting old 

  • Decreased metabolic rate

• Cognitive changes:

  • Fatigue and lethargy

  • Impaired memory

  • Low initiative

  • Weight gain:

    • Intolerance of exercise

  • Changes in personality:

    • Personality and mood changes

    • Depressed 

  • Slowed speech

  • Somnolence:

    • Sleepiness

  • Decreased appetite

  • Shortness of breath

• Older adult:

  • Fatigue

  • Cold

  • Dry skin

  • Hair loss

  • Constipation

Hypothyroidism cv and skin manifestations 

• Cardiovascular:

  • CV problems may be significant in patients with history of cardiovascular disease

  • Decreased cardiac contractility and output

  • Anemia

  • Increased serum cholesterol and triglycerides:

    • Worse for those with atherosclerosis

    • Thyroid hormones stimulate lipid metabolism:

      • No thyroid hormone = no lipid metabolism

• Integumentary: VERY DRY BUT BECOMING A SNOWMAN ⛄

  • Dry, thick, inelastic, cold skin

  • Thick, brittle nails

  • Dry, sparse, coarse hair

  • Poor turgor of mucosa

  • Generalized interstitial edema

  • Puffy face

  • Decreased sweating

  • Intolerance to cold

  • Pallor

• Myxedema:

  • Accumulation of mucopolysaccharides within the dermis/tissue:

    • Look puffy/skin is mushy

Hypothyroidism complications 

• Myxedema coma

Hypothyroidism meds + patient teaching

• IV thyroid hormone:

  • Control BP

  • Breathing

  • Warm their temperature

• Diagnostic studies = Thyroid hormones, cholesterol, triglycerides, anemia, and creatine kinase  

• Medications: 

  • Levothyroxine/Synthroid:

    • Start with low dose, check every 4-6 weeks of thyroid hormones 

      • To prevent thyroid storm

    • Monit 

      • Signs of hyperthyroidism:

        • Chest pain

        • Weight loss

        • Nervousness

        • Tremors

        • Insomnia

    • Increase dose in 4 to 6 week intervals as needed based on TSH levels

    • Lifelong therapy

    • Can not switch from generic to trade:

      • Vice versa

• Patient teaching:

  • Written instructions important

  • Take medication on an empty stomach in the morning, 30 mins before eating 

  • Need for lifelong therapy (forever), need to adhere to this therapy.

  • Avoid abruptly stopping drugs - never do that 

  • Side effects of medication

    • Can not switch brands of medication

  • Teach s/sx of hypotension/hyperthyroidism

Myxedema Coma

• The body's metabolic demand increases, but because there is a severe deficiency of thyroid hormones, the body is unable to respond appropriately to the stress:

  • Precipitated by infection, drugs, colds and trauma

• Characterized by: more severe signs of hypothyroidism 

  • Impaired consciousness

  • Subnormal temperature

  • Hypotension

  • Hypoventilation

  • Cardiovascular collapse

Thyroid cancer 

• Thyroid nodule can be benign or malignant, watch for tracheal compression 

• Most common type of endocrine cancer, higher risk in women, whites, asian americans, exposure to head/neck radiation therapy, radioactive fallout, and f/x of goiter 

• Papillary = grows slowly, spreads to lymph nodes

• Follicular = in older adults, that metastasizes in cervical lymph nodes then spread to neck, lungs, and bones

• Medullary = in families and associated with other endocrine problems, diagnosed with test looking for RET gene 

• Anaplastic = most advanced and aggressive cancer, poor prognosis 

• Manifestations = Painless palpable nodule/nodules (firm, palpable masses suggest metastasis), trouble swallowing/breathing, hemoptysis, air-way obstruction   

• Tests = CT, MTI, FNA ultrasound (hot- benign vs cold- high risk for being cancer), serum calcitonin levels, and genetic testing 

• Treatment = Total/bilateral lobectomy, RAI therapy, external beam radiation, thyroid hormone therapy, chemotherapy, targeted therapies

• Assess patient for airway obstruction, bleeding, and tetany

Multiple endocrine neoplasia (MEN)

• Inherited condition by hormone secreting tumors 

• Mutation of MEN1 or RET  

• Type 1 = parathyroid gland hyperactivity, prolactinoma, and gastrinoma 

• Type 2 = medullary thyroid carcinoma, pheochromocytoma (tumor of adrenal glands) 

• Treatment includes conservative management (watchful waiting), drugs to block the effects of excess hormone, and surgical removal of the gland and/or tumor 

🐹Diabetes Mellitus

• A chronic multisystem disease characterized by hyperglycemia related to abnormal insulin production, impaired insulin use or both 

• Affects 34.2 million people in the United States:

  • 6 million in 2.5 years:

    • 17.3 million unaware 

    • 88 million have prediabetes

• 7th leading cause of death BUT major contributor to CVD which is #1 cause of death 

• Blindness due to retinopathy and leg amputation   

🐹Diabetes Mellitus etio and patho

• Theory of causes single or combination of factors:

  • Genetic

  • Autoimmune

  • Environmental 🍔- eating habits o b e s i t y, lack of exercise -> metabolic syndrome

• The American Diabetes Association/ADA recognizes four different classes of diabetes:

  • Type I

  • Type II

  • MODY = maturity onset diabetes of the young 

  • Gestational:

    • Pregnancy

  • Other:

    • Chronic pancreatitis

    • Pancreatic cancer;

      • Leads to DM

  • Normal glucose range = 74 - 106 mg/dL  (4.1 to 5.9 mmol/L) 

  • Normal insulin excreted daily is 40-50 U or 0.6 U/kg of body weight 

  • *Measuring C-peptide in serum and urine is useful indicator of pancreatic B-cell function and insulin levels 

Comparison of Type I and Type II DM

Factor	Type I	Type II
Age of onset	Any age but more common in young people	Adults Increased incidence in children
Type of onset	Abrupt but may have been present many years	Insidious (may people unaware they have DM
Prevalence	5-10%	90-95%
Environmental factors	Virus, toxins	Obesity, lack of exercise
Primarily defect	Absent of minimal insulin production	Insulin Resistance (insulin not being used/ineffective use) -Decreased production -Altered adipokines
Islet cell antibodies	Present at onset	Absent
Endogenous insulin	Absent	Initially increased, then secretion decreases
Nutrition	Thin, normal or obese	Frequently overweight or obese May be normal
Symptoms	Polyuria Polydipsia Polyphagia Fatigue Weight Loss	None Recurrent infection Fatigue Polyuria Polydipsia Polyphagia
Ketosis	Prone at onset or during insulin deficiency	Resistant except with infection or stress
Nutrition	Essential	Essential
Insulin	Required for all	Required for some; may progress to need it
Vascular and neurologic complications	Frequent	Frequent

Type I Diabetes

• An autoimmune disease that leads to the destruction of beta cells:

  • Stops insulin production:

    • Treatment is to replace insulin

• Formerly known as juvenile-onset or insulin-dependent diabetes

• Accounts for about 5 to 10% of all people with diabetes

• Generally affects people under the age of 40:

  • Can occur at any age 

  • Ex: Latent autoimmune diabetes 

  • Inheritance = Idiopathic diabetes 

Type I Diabetes patho

• Islet cell autoantibodies present for months to years before onset of symptoms

• Manifestations develop when pancreas can no longer make enough insulin:

  • Rapid onset of ketoacidosis:

• Requires exogenous insulin

• Patient may have temporary 3 to 12 months remission after starting treatment

• Ketones released which leads to acidosis:

  • Leads to Diabetic KetoAcidosis/DKA:

    • Abdominal pain

    • N/V

    • Hyperventilation

    • Fruity odor breath

    • Neuro changes:

      • LOC

      • Coma

      • Death

  • Decreased insulin:

    • Leads to increase glucose serum (glucose is not used):

      • Leads to increased fat metabolism:

        • Releases ketones

Type I Diabetes manifestations + treatment

• Classic symptoms:

  • Polyuria

  • Polydipsia

  • Polyphagia

• Weakness

• Fatigue

• Ketoacidosis:

  • Weight loss

• Treatment:

  • Replace insulin because pancreas is no longer capable of producing (at first little as there are healthy glucose levels but will soon need more as b-cells are destroyed  

  • Check the blood glucose level every 2 to 4 hours

Type II Diabetes

• Formerly known as adult-onset diabetes or non-insulin-dependent diabetes

• Most prevalent type:

  • 90 to 95%

• Many risk factors:

  • Overweight

  • Obese

  • Advanced age 

  • Family history 

    • Increased prevalence in children due to obesity

• Greater prevalence in ethnic groups:

  • African Americans

  • Hispanics

Type II Diabetes etio and patho

• Pancreas usually makes some endogenous insulin but:

  • Not enough insulin is produced and/or increased glucose production

  • Body does not use insulin effectively

  • Insulin resistance:

    • Tissue becomes less sensitive to insulin:

      • Pancreas works hard to produce more insulin:

        • Issue with insulin production or use of insulin

      • Inappropriate glucose production by liver 

      • Production of hormones and cytokines, adipokines 

• Major distinction:

  • Presence of endogenous insulin

  • In type I diabetes, there is an absence of endogenous insulin

• Metabolic syndrome increases risk for type 2 DM:

  • Increased glucose levels

  • Abdominal obesity

  • High BP

  • High triglyceride levels

  • Decreased HDLs levels:

    • 3 of 5 components:

      • Metabolic syndrome

Type II Diabetes onset

• Gradual onset:

  • S/Sx when there is target organ damage:

    • Kidney disease

• Person may go many years with undetected hyperglycemia

• Often discovered with routine laboratory testing:

  • High glucose or hemoglobin A1C

• Prediabetes = 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 mg/dL (7.8 to 11.0 mmol/L).

• - IFG is diagnosed when fasting glucose levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L) 

• Gestational diabetes = Those at high risk include women who are obese, are of advanced maternal age, or have a family history of DM. We screen women with an average risk for gestational DM using an OGTT at 24 to 28 weeks of gestation 

  • At time of diagnosis:

    • About 50% to 80% of beta cells are no longer secreting insulin

    • Average person has had diabetes for 6.5 years without knowing

Type II Diabetes manifestations + treatment

• 3Ps: (not necessarily always present)

  • Polydipsia 

  • Polyphagia

  • Polyuria

• Nonspecific Symptoms:

  • Classic symptoms of type I may manifest

• S/Sx:

  • Fatigue

  • Recurrent infection

  • Recurrent vaginal yeast or candida infection (fungal)

  • Prolonged wound healing

  • Visual problems

• Treatment:

  • First line treatment:

    • Diet

    • Exercise = losing weight and helps with BP and hyperlipidemia 

    • Hypoglycemics

      • Eventually end up on insulin

Diabetes diagnostic studies criteria

• A1C level:

  • 6.5% or higher

• Fasting Plasma Glucose/FPG level:

  • Diabetes:

    • x>126 mg/dL

  • Prediabetes:

    • 100-125 mg/dL

• 2-hour plasma glucose level during OGTT/Oral Glucose Tolerance Test greater than 200 mg/ dL:

  • With glucose load of 65g

• Repeat criteria 1 to 3 on another visit to confirm

• Be attentive to influencing factors:

  • Classic symptoms of hyperglycemia or hyperglycemic crisis or a random plasma glucose level greater than 200 mg/dL

Types of Diabetes tests

• A1C:

  • Diabetes:

    • Over 6.5%

• Glycosylated Hemoglobin:

  • Reflects glucose levels over past 2 to 3 months

  • Glucose attaches to hemoglobin molecule:

    • The higher the glucose levels the higher the A1C

    • Does not consider the glucose fluctuations as other diseases affect RBCs and A1C

  • Used to:

    • Diagnose

    • Monitor response to therapy

    • Screen patients with prediabetes

• Goal:

  • Less than 6.5% to 7%:

    • Reduces complications

• Fructosamine =  chemical reaction of glucose with plasma protein 

- Reflects previous 1-3 weeks 

- used for people with hemoglobinopathies or short-term mea- surement of glucose levels, for instance, after a change in medi- cation or during pregnancy

- Islet cell autoantibody testing can help distinguish between autoimmune type 1 DM and DM from other causes 

Diabetes goals

• Reduce symptoms

• Promote well-being

• Prevent acute complications

• Prevent or delay onset and progression of long-term complications

• Normalize insulin/glucose level

• Meeting goals of ABCs of diabetes lowers risk of heart attack:

  • A1C

  • BP

  • Cholesterol

Diabetes drug therapy

• Insulin:

  • Exogenous injected insulin:

    • Insulin from outside source

    • Multiple daily injections or insulin pump:

      • Monitor glucose levels closely

    • Required for type 1 diabetes

    • Prescribed for patients with type 2 diabetes during times of stress or as disease progresses and unable to manage glucose levels with previous therapies

  • Types = rapid-acting, short-acting, intermediate-acting, and long-acting insulin

  • Basal-bolus plan = multiple daily insulin injections or insulin pump together with frequent BGM or CGM to achieve a glucose level close to normal (time in range) 

- Bolus = Mealtime insulin including Aspart, Glulisine, Lispro

- Basal = in between meals and nighttime including degludec, determir, and glargine 

  - Insulin storage = out of the sun, must be left in room temp up to 4 weeks but cannot go higher than 86F or below 32F, warm the syringe and in vertical position before injection 

  - Administration = subcutaneous injection, no air bubbles, and caution the site that will be exercised as it can increase rate of insulin

- fastest subcutaneous absorption is from the abdomen, followed by the arm, thigh, and buttock 

- Injected at 90 degree angle and available as U100 (1 mL per 100 U of insulin) 

- Other devices = OmniPod, Insulin pump

Insulin issues

• Allergic reaction = urticaria, anaphylactic shock

• Lipodystrophy = changes in subcutaneous fatty tissue like atrophy (if same injection sites are used) and hypertrophy (erratic insulin absorption)  

• Somogyi Effect

• Dawn Phenomenon

Somogyi Effect

• High dose of insulin cause decreased glucose during the night:

  • Causing the body to release of counterregulatory hormones (glucagon) which causes rebound hyperglycemia (increased glucose)

• The body reacts to a hypoglycemic episode by releasing stress hormones which stimulate the liver to release stored glucose causing an increase in blood glucose levels.

• Dangers:

  • When glucose checked in the morning and increased insulin is given

Somogyi Effect preventation and treatment

• Prevention:

  • Determine if there is Somogyi effect by checking glucose between 2 to 4 A.M:

    • Assess patient for headache, night sweats or nightmares

• Treatment:

  • Bedtime snack

  • Reducing the dose of insulin 

Dawn Phenomenon

• Morning hyperglycemia present on awakening

• May be due to release of counterregulatory hormones in predawn hours:

  • Growth hormone and cortisol increases glucose levels:

    • GH and cortisol wakes us up from sleep 

  • More severe in adolescence and young adulthood:

    • Peak time for growth hormone

• Treatment:

  • Increase in insulin 

  • Adjustment of administration time

Other types of insulin

• Inhaled insulin = Afrezza is rapid acting inhaled insulin used in combination with long-acting insulin for DM type 1 (bronchospasm, hypoglycemia, cough, and throat pain/irritation)

• Oral and Non-Insulin Injectable Agents:

  • Work to improve the mechanisms by which the body makes and uses insulin and glucose

  • Work on 3 defects of type 2 DM:

    • Insulin resistance

    • Decreased insulin production

    • Increased hepatic glucose production

  • Can be used in combination drugs from other classes or with insulin 

  • Ex = Biguanides (Metformin), Sulfonylureas, Meglitinides, a-Glucosidase inhibitors, Thiazolidinediones, Dipeptidyl peptidase-4 inhibitors, SGLT2 inhibitors, Dopamine receptor agonist, GLP-1 receptor, and amylin analogs

Other meds for diabetes

• Medication:

  • Increases release from pancreas:

    • Sulfonylureas:

      • Loses their potency and patients will eventually be on insulin

• Increases in insulin production

• Decrease in the production of glucagon from liver

• Biguanides:

  • Metformin/Glucophage:

    • Given for patients with prediabetes

    • Most effective 1st line treatment for type 2:

      • Available as immediate release, extended release and liquid forms

    • Action:

      • Reduces glucose production by liver

    • Enhances insulin sensitivity

    • Improves glucose transport

    • May cause weight loss

    • Used in prevention of type 2 diabetes

• Alerts:

  • Withhold if patient is undergoing surgery or radiologic procedure with contrast medium:

    • 24 to 48 hours before and at least 48 hours after when serum creatinine is within normal limits:

      • Affects the kidneys 

• Contraindications:

  • Renal, Liver, Cardiac disease:

    • Lactic acidosis

  • Iodine based contrast medium can cause AKI

  • Excessive alcohol intake

Nutrition Therapy for diabetes

• Done with exercise and monitor blood glucose

• ADA Guidelines:

  • Person with DM can eat the same foods as without DM (in moderation)

  • Overall goal:

    • Achieve and maintain safe and healthy glucose levels

  • Prevent or reduce the risk of complications

  • Achieve lipid profiles and BP that reduce risk for CVD

  • Prevent or slow development of chronic complications

  • Individual needs; personal and cultural preferences

  • Maintain pleasure of eating with healthy choices

• MyPlate Guidelines:

  • 9’ inch plate:

    • ½ non starchy vegetables

    • ¼ starch

    • ¼ protein -> lean protein 

    • 8 oz of nonfat milk 

    • Small piece of fruit 

    • Fiber = 14 g per 1000 kcal 

    • Healthy fats = olives, nuts, and avocados 

    • Moderate alcohol use, 2 for men and 1 for women

  • Carb counting depending on glucose levels, age, weight, activity level, patient preference, and drug plan 

  • Diabetes exchange list = encourage well-balanced meal plan 

  • Exercise at least 150 minutes/week, have a 10-15 g carb snack to prevent hypoglycemia  

Patient edcuation on monitoring blood glucose

• Blood Glucose Monitoring/BGM:

  • Enables decisions about food intake, activity patterns and medication dosages

  • Accurate record of glucose fluctuations and trends

  • Recommended for all diabetics who use insulin and others to help achieve and maintain glycemic goals

  • BGM use portable blood glucose meters and CGM systems 

• Patient and Caregiver Teaching:

  • Initial and follow-up:

    • Instructions how to test, use and calibrate meter

  • When to test:

    • Before meals

    • Two hours after first bite

    • When hypoglycemia is suspected

    • Every 4 hours during illness

    • Before and after exercise

      • Usually check every 2 to 4 hours

Surgical Treatment for diabetes

• Pancreatic Beta Cells Transplant:

  • A pancreatic beta cell transplant is a form of cellular transplantation that aims to restore insulin production in people with Type 1 diabetes

- Pancreas transplantation

• 3 criteria: (1) a history of frequent, acute, and severe metabolic complications (e.g., hypoglycemia, hyperglycemia, DKA) requiring medical attention; (2) clinical and emotional problems with the use of insulin therapy that are so severe as to be incapacitating; and (3) consistent failure of insulin-based management to prevent acute complications 

• Will need lifelong immunosuppressive therapy 

    

• Bariatric Surgery:

  • Bariatric surgery refers to a range of surgical procedures that are performed to treat obesity. In individuals with Type 2 diabetes (T2D)

Nursing care for diabetes

• Patient needs to know about their glucose range, effects of insulin, food, stress and exercise: Normal glucose levels is 70 to 110

  • Pre-meal:

    • 70-130

  • Post-meal:

    • x<80

• ID bracelet to identify that they have DM

• Recognize/Treat hypoglycemia and hyperglycemia

• Administer insulin

• Monitor glucose

• Determine if acute/chronic or DKA

  • Monitor K⁺ levels and rehydrate patient

• Enable the patients to become active participants in the management of their disease

Acute Complications of diabetes

• Hypoglycemia

• Hyperglycemia

• Diabetic KetoAcidosis/DKA

• Hyperosmolar Hyperglycemic Syndrome/HHS

Hypoglycemia

• Too much insulin in proportion to glucose in the blood:

  • Missing a meal

  • Overdosing

  • Exercise/Exertion

• Glucose level x<70 mg/dL

• Patients are often unaware:

  • No warning signs/symptoms until glucose level critically low:

    • Incoherent, combative, loss of consciousness

  • Related to diabetes-related autonomic neuropathy and increased secretion of counterregulatory hormones

  • Patient at risk should keep glucose levels somewhat higher

• Patients are often unaware/ hypoglycemic unawareness:

  • No warning signs/symptoms until glucose level critically low

    • Incoherent, combative, loss of consciousness

  • Related to diabetes-related autonomic neuropathy and increased secretion of counterregulatory hormones

  • Patient at risk should keep glucose levels somewhat higher

Hypoglycemia patho

• Neuroendocrine hormones released:

  • Autonomic nervous system activated:

    • Epinephrine released:

      • Response to hypoglycemia

      • Epinephrine stimulates glycogenolysis and insulin inhibition

Hypoglycemia manifestations pt 1

• Epinephrine released: Adrenergic symptoms = everything is high 

  • Pallor

  • Diaphoresis

  • Tremors/Shakiness

  • Palpitations

  • Tachycardia

  • Nervousness/Anxiety

  • Hunger:

    • Due to low glucose

    • Stimulation of SNS

  • CNS changes:

    • Headache

    • Confusion

    • Vision changes:

      • Dizziness

    • Double vision

    • Changes in LOC

    • Drowsiness

    • Inability to concentrate

      • Due to low glucose in the brain

Hypoglycemia manifestations pt 2

• Altered mental function/Neuroglycopenia:

  • Difficulty speaking

  • Visual disturbances

  • Stupor

  • Confusion

  • Coma

  • Mimics alcohol intoxication

• Untreated hypoglycemia can progress to:

  • Loss of consciousness (LOC)

  • Seizures

  • Coma

  • Death

• Others:

  • Blood glucose x<70 mg/dL

  • Cold, clammy skin

  • Numbness fingers, toes and mouth

  • Faintness

  • Unsteady gait

  • Slurred speech

Hypoglycemia treatment

• Rule of 15:

  • Consume 15 g of a simple carbohydrate:

    • Fruit juice or regular soft drink:

      • 4 to 6 oz

    • Commercial products:

      • Gel or tablets

    • In hospital:

      • Dextrose IV push

    • Type 1:

      • Carry glucagon when glucose decreases

• Recheck glucose level in 15 minutes:

  • Repeat if still <70g/dL:

    • If remains low after 2 or 3 times:

      • Contact HCP

  • If glucose is stable; give carb and protein

• Avoid food with fat:

  • Slows glucose absorption

• Avoid overtreatment

• Acute Care:

  • 50% dextrose 20 to 50 mL IV push:

    • Patient not alert enough to swallow or no IV access; also teach family/caregiver

• Glucagon 1 mg IM or subcutaneously:

  • Watch for nausea:

    • Prevent aspiration

  • May not be effective with:

    • Alcohol-related liver disease

    • Starvation

    • Adrenal Insufficiency

• Explore reason why it occurred

Diabetic KetoAcidosis/DKA

• The body produces high levels of blood acids called ketones:

  • Body breaks down fat as an alternative energy source:

    • Since insulin insufficiency or resistance, glucose does not enter the cells

• Caused by profound deficiency of insulin

• Most likely to occur in type I diabetes

• May occur in people with type II DM with severe illness or stress

• Characterized by:

  • Hyperglycemia

  • Ketosis

  • Acidosis

  • Dehydration

  • Fruity odor breath

Diabetic KetoAcidosis/DKA main features + manifestations

• Main clinical features:

  • Insulin deficiency:

    • Leads to hyperglycemia

  • Hypovolemia:

    • Fluid and electrolyte loss:

      • Excess glucose pulls on water as it is urinated

      • Shock and renal failure 

  • Acidosis

  • Hypokalemia:

    • Potassium is pulled out of the body by glucose when urinating

• Clinical manifestations 

- Dehydration, tachycardia, orthostatic hypotension 

- Lethargy and weakness (early signs) 

- Eyes become soft and sunken 

- Abdominal pain, anorexia, nausea, vomit, fruity odor 

- Kussmaul respirations 

Diabetic KetoAcidosis/DKA treatment

• IV insulin drip -> obtain K+ levels beforehand 

• IV infusion of 0.45%/0.9% NaCl and Dextrose 5 or 10%

• Fluids

• Medications for acidosis

Hyperosmolar Hyperglycemic Syndrome/HHS

• Involves extreme dehydration and hyperosmolarity:

  • No ketoacidosis

• Seen in Type II DM:

  • Able to make enough insulin to prevent DKA, but still have severe hyperglycemia, osmotic diuresis and ECF depletion:

    • Missing the acidosis like in DKA

• More severe than DKA

• Life-threatening syndrome:

  • Less common than DKA

Hyperosmolar Hyperglycemic Syndrome/HHS patho

• Enough circulating insulin to prevent ketoacidosis:

  • Ketones absent or minimal in blood and urine

• Fewer early symptoms lead to higher glucose levels: slow onset

  • Greater than 600 mg/dL

• More severe neurologic manifestations because of increased serum osmolality

Hyperosmolar Hyperglycemic Syndrome/HHS manifestations

• Somnolence

• Coma

• Seizures

• Hemiparesis:

  • Paralysis on 1 side of the body

• Aphasia

• Similar to stroke

Hyperosmolar Hyperglycemic Syndrome/HHS interprofessional care

• Correct underlying precipitating cause

• Medical emergency:

  • High mortality rate

• Management similar to DKA:

  • IV insulin and NaCl infusions:

    • Add dextrose when glucose levels:

      • 250 mg/dL:

        • Reduce it gradually

  • More fluid replacement needed:

    • Hemodynamic monitoring to avoid overload

• Monitor:

  • Fluid and electrolytes:

    • K⁺:

      • Hypokalemia

  • Serum osmolality

  • Vital signs 

  • Input and output

  • Skin turgor

  • Neuro status

  • Renal status

  • Cardiac status

DKA/HHS nursing care

• Monitor:

  • Glucose

  • Urine for output

  • IV fluids

  • Insulin therapy

  • Electrolytes:

    • K⁺

• Assess:

  • Renal status

  • Cardiopulmonary status

  • Level of consciousness

Long-Term Complications of Diabetes

• Stroke

• HTN

• Dermopathy

• Atherosclerosis:

  • Peripheral vascular atherosclerosis

• Nephropathy

• Peripheral neuropathy:

  • Numbness

  • Tingles

• Neurogenic bladder

• Erectile dysfunction

• Infections

• Gangrene

• Islet cell loss

• Gastroparesis

• CAD

• Retinopathy

• Cataracts

• Glaucoma

• Blindness

• Angiopathy:

  • Leading cause of death

  • Damage to blood vessels

Angiopathy

• Damage to blood vessels secondary to chronic hyperglycemia

• Leading cause of diabetes-related death:

  • 68% cardiovascular disease

  • 16% stroke

    • Age 65 and older

• Possible causes include

• (1) the accumulation of damaging by-products of glucose metabolism, such as sorbitol, which damage nerve cells

• (2) the formation of abnormal glucose molecules in the basement membrane of small blood vessels, such as those that circulate to the eyes and kidneys; and

• (3) a problem with RBC function that leads to a decrease in tissue oxygenation

Angiopathy types

• Macrovascular:

  • Disease of large and medium-sized blood vessels:

    • Cerebrovascular disease

    • Cardiovascular disease

    • Peripheral vascular disease

      • All lead to stroke and heart attack

• Greater frequency and earlier onset in patients with diabetes:

  • Women 4 to 6 times risk for cardiovascular disease

  • Men 2 to 3 times risk for cardiovascular disease in those nondiabetics

• BP screening at every visit for people with BM, plus lifestyle counseling for BP greater than 130/80 mm Hg and treatment to achieve BP of less than 140/90

• Microvascular:

  • Thickening of vessel membranes in capillaries and arterioles from chronic hyperglycemia

  • Areas most affected:

    • Eyes:

      • Retinopathy

    • Kidneys:

      • Nephropathy

    • Nerves:

      • Neuropathy

Retinopathy

• Microvascular damage to retina 

• Nonproliferative = partial occlusion of small blood vessels in retina where capillary fluid leaks causing retinal edema, retinal hemorrhages, and vision loss

• Proliferative = retinal capillaries become occluded, so body forms new blood vessels (neovascularization) that are fragile and bleed easily causing vitreous contraction and black/red spots or lines thus can lead to blindness due to detachment of retina 

• Other factors = Glaucoma and Cataracts 

• Treatment = Maintain glucose and BP levels, eye exam, laser photocoagulation (promotes neovascularization), vitrectomy (aspiration of blood), and Iluvien (injectable treatment) 

Nephropathy

• Damage to small blood vessels that supply the glomeruli of the kidney

• Leading cause of end-stage renal disease in US:

  • 20 to 40% of people with diabetes have it

• Risk factors:

  • HTN

  • Genetics

  • Smoking

  • Chronic hyperglycemia (also leaking into the urine too)

• Screen of random spot urine collection to assess for albuminuria and albumin to creatinine ratio 

• Treatment = ACE inhibitor, ARBs 

Neuropathy

• Nerve damage due to metabolic imbalances of diabetes:

  • 60 to 70% of patients with diabetes have some degree of neuropathy

  • Sensory neuropathy:

    • Most common

    • Loss of protective sensation in lower extremities:

      • Increases risk of amputation

      • 60% of nontraumatic amputation is related to diabetes 

    • Pain 

    • Paresthesias:

      • Tingling

      • Burning

      • Itching

      • Walking on pillows or numb feet

    • Very sensitive to touch:

      • Hyperesthesia

    • Complete or partial loss of sensitivity to touch or temperature is common

    • Foot injury and ulcerations may occur without patient ever having pain

    • Small muscles of hand and feet may be affected causing deformity and limited fine movement (atrophy) 

  • Treatment = Manage glucose levels, topical creams (e.g., capsaicin), tricyclic antidepressants (e.g., amitriptyline), selective serotonin and norepinephrine reuptake inhibitors (e.g., duloxetine), and antiseizure drugs (e.g., gabapentin)

Autonomic Neuropathy

• Affect nearly all body systems and lead to hypoglycemia unawareness, bowel incontinence, diarrhea, and urinary retention 

• Systems:

  • In GI:

    • Slowing down of peristalsis:

      • Gastroparesis

      • Anorexia, nausea, vomiting, reflux, and feelings of fullness

  • In heart:

    • Painless MI

    • Postural hypotension

    • Resting tachycardia 

  • Other systems = Erectile dysfunction, neurogenic bladder 

• Screen:

  • Type II:

    • Time of diagnosis

  • Type I:

    • 5 years after diagnosis

Foot and Lower Extremity Complications + diabetes

• High risk of foot ulcerations and lower extremity amputations 

• Microvascular (neuropathy) and macrovascular (peripheral artery disease) increases risk for injury and injection:

  • Sensory neuropathy and PAD are major risk factors:

    • Prevents patient from being aware an injury has occured 

    • Leads to poor wound healing due to poor perfusion

    • Signs = intermittent claudication, pain at rest, cold feet, loss of hair, delayed capillary refill, and dependent rubor 

  • Other factors:

    • Clotting abnormalities

    • Impaired immune function

    • Autonomic neuropathy

  • Smoking increases risk

  • Neuropathic arthropathy, or Charcot’s foot, results in ankle and foot changes that lead to joint problems and footdrop. These changes occur gradually. They promote an abnormal distribution of weight over the foot. This increases the chances of developing a foot ulcer as new pressure points appear 

Skin complications + diabetes

• DM-related dermopathy = skin lesion that is reddish-brown, round/oval patches 

• Acanthosis nigricans = manifestation of insulin resistance that is light brown to black skin thickening on flexures, axillae, and neck 

• Necrobiosis lipoidica diabeticorum = red-yellow lesions with atrophic skin that becomes shiny and transparent revealing tinting blood vessels under the surface 

Infection with diabetes

• Defect in mobilization of inflammatory cells and impaired phagocytosis (WBC, neutrophil, and monocyte):

  • Recurring or persistent infections:

    • C. Albicans

    • Boils

    • Furuncles

    • Cystitis

  • Persistent glycosuria predispose people to bladder infection and angioplasty prevent/delay immune response

• Treatment:

  • IV Antibiotics:

    • Prompt and vigorous

• Educate patient on infection prevention:

  • Hand hygiene

  • Avoid exposure

  • Flu and pneumococcal vaccine

Psychological and Gernotolgic Consideration with diabetes 

• High rates of:

  • Depression

  • Anxiety

  • Eating disorders

• Diminished self care

• Helplessness

• Poor outcomes

• Diabetes distress:

  • Stress

  • Fear

  • Burden of living with and managing diabetes 

• Disordered eating behaviors

Gerontologic Considerations:

• Increased prevalence and mortality:

  • Present in 25% over age 65 due to reduced beta cell function, decreased insulin sensitivity and altered carbohydrate metabolism

  • Higher rate of death, functional disability (renal dysfunction) and coexisting illnesses

  • More drugs that interfere with insulin action

  • Many undiagnosed and untreated:

    • Signs resemble changes associated with aging

  • Unable to administer insulin or check glucose

Head injury

• Any trauma to:

  • Scalp

  • Skull

  • Brain

• Traumatic Brain Injury/TBI:

  • Mostly due to accidents

• High incidence

• Use the Glasgow Coma Scale/GCS:

  • Helps distinguish between the types of brain injury

  • Highest level is 15

  • Less than 8 need ventilation

Head injury etio

• Common causes:

  • Falls

  • Motor vehicle accidents

• Other causes:

  • Firearms

  • Assaults

  • Sports-related trauma

  • Recreational injuries

  • War-related injuries

Scalp lacerations

• External head trauma

• Scalp is highly vascular which can cause profuse bleeding

• Major complications:

  • Blood loss

  • Infection

Skull fractures

• A break in the skull bone resulting from a significant head injury:

  • Can cause permanent damage to brain tissue

• Location of fracture determines s/sx

• Types:

  • Appearance:

    • Linear:

      • A linear skull fracture is a single, thin crack in the skull, often running in a straight line.

    • Depressed:

      • Part of the skull is pushed inward toward the brain, creating an indentation.

• Structure and Severity:

  • Simple:

    • A simple skull fracture is a break in the bone without any damage to the skin or surrounding tissue.

• Comminuted:

  • The bone is shattered into three or more pieces.

• Compound:

  • An open fracture where there is a break in the skull along with an overlying skin laceration, exposing the brain or skull.

• Skin:

  • Closed:

    • The skin over the fracture remains intact, meaning there is no open wound.

  • Open:

    • An open fracture involves a break in both the skull and the overlying skin

• Complications:

  • Hematoma:

    • Internal bleeding:

      • Increases pressure due to displaced space by the bleeding:

        • Brain herniation

        • Infection

Concussion Injury

• A type of diffuse injury – injury in all areas of the brain:

  • Sudden transient mechanical injury

  • Brief disruption in LOC

    • Glasgow Coma Scale/GCS

  • Retrograde amnesia

  • Headache

  • Short duration

  • May result in postconcussion syndrome:

    • 2 weeks to 2 months after injury:

      • Headache

      • Lethargy

      • Shorted attention span and decreased short-term memory 

      • Changes in:

        • Intelligence

        • Behavior

        • Personality

Diffuse axonal injury

widespread axonal damage after TBI

- trauma changes function of axon -> swelling and disconnection

- Manifestations = decreased LOC, increased ICP, decortication/decerebration, and global cerebral edema 

Lacterations 

 type of focal injury -> actual tearing of brain tissue 

- occur in depressed and open fractures/penetrating injuries 

- Initial treatment is antibiotics and preventing secondary injury from increased ICP 

- Manifestations = bleeding, hematoma, seizures, and cerebral edema

Contusion

• A type of focal injury – occurs at the site of the fracture:

  • Bruising of brain tissue

  • Associated with closed head injury

  • May continue to bleed or rebleed

  • Monitor for seizures

  • Potential for increased hemorrhage if on anticoagulants 

  • May have areas of:

    • Hemorrhage

    • Infarction

    • Necrosis

    • Edema

    • Seizures (common) 

    • Blossoming:

      • Rebleeding of original contusion:

        • Now have larger area of damage

Coup-Contrecoup Injury

• Makes up:

  • Coup:

    • Occurs at the site where the head is directly impacted

• Contrecoup:

  • Occurs on the opposite side of the brain from the initial impact

    • Multiple areas damaged 

  •   brain stem and spine 

More severe and damage depends on how much bleeding

Signs of head injury + treatment

• Raccoon Eyes:

  • Bruising or dark discoloration around both eyes

  • Occurs in linear fractures

• Battle’s Sign:

  • Bruising or dark discoloration behind one or both ears

  • Occurs in linear fractures

  • CSF leak in ear:

    • Leakage in one nostrils

• Treatment for both:

  • Presence of hematoma and depressed fracture:

    • Open skull surgery or craniotomy

    • Need to repeatedly check the pt LOC.

Epidural Hematoma

• Bleeding between the dura and inner surface of the skull

• Neurologic emergency

  • The skull does not expand, so we need to relieve the pressure. 

• Venous origin = slow

• Arterial origin = rapid and bleed faster 

• Changes in LOC:

  • Initially unconscious:

    • Leads to lucid:

      • Then rapid reduction level of consciousness 

• S/Sx:

  • N/V

  • Headaches

• Treatment:

  •  Surgery:

    • CAT scan right after

• Burr hole done to relieve hematoma

Subdural Hematoma

• Between the dura mater and the arachnoid mater

• Acute (within hours), subacute (2-14 days), or chronic (weeks to months, brain atrophy)

• S/Sx:

  • Changes in LOC = drowsy and confused 

  • Headache 

  • Fixed dilated pupils if ICP increases 

• Treatment:

  • Surgical drainage

Subarachnoid Hematoma

• Between the arachnoid mater and the pia mater in the subarachnoid space, which contains CSF

• S/Sx:

  • Sudden onset of a severe headache

  • Neck stiffness and sensitivity to light

  • N/V

  • Changes in LOC

  • Thunderclap headache

• Treatment:

  • Surgical clipping or endovascular coiling of an aneurysm

• Intracerebral hematoma = bleeding within the brain, rupture of intracerebral vessels 

Emergency Treatment of head injury

• CT scan, MRI, PET, doppler studies, and cervical spine x-ray

• Craniotomy = use for depressed fractures and loose fragments fractures  

• Craniectomy = large amounts of bone are destroyed, extreme swelling, bleeding

• Burr-hole = rapid decompression 

• ABCs

• Stabilize cervical spine

• Oxygen

• IV access

• Intubate if GCS less than 8

• Control external bleeding

• Remove patient’s clothing

• Complication:

  • Secondary injury:

    • Occurs as a normal body response to primary injury:

      • Cerebral edema due to inflammatory process:

        • Increases ICP:

          • Results in more damage and could be fatal

Head injury objective data assessment

• Altered mental status

• Lacerations, contusions, abrasions

• Hematoma

• Battle’s signs

• Raccoon eyes

• Periorbital edema and ecchymosis

• Otorrhea (ear) = CSF leak 

• Rhinorrhea (nose) = CSF leak 

- Risk of meningitis so give antibiotics right away

- Dextrostix or test-tape strip for glucose or look for halo/ring sign when leaking fluid drip onto white gauze pad

• Exposed brain

• CSF leakage

• Gag reflex, seizure, incontinence

• Signs of:

  • Cushing triad

  • Impending brain herniation

*Medications = anticoagulant, blood thinners -> bleeding

Neuro assessments/tests for head injury

• Do frequently

• Use GCS

• Immediate CAT scan:

  • Detect bleeding:

    • MRI:

      • Takes longer and inside the tube – can not see the patient

• Check for increased ICP

• Blood test for any toxicity like drugs or alcohol 

• EEG

Head injury goals

• Goals:

  • Patient will:

    • Maintain adequate cerebral oxygenation and perfusion

    • Stay afebrile

    • Be free of discomfort/pain

    • Be free from infection

    • Have adequate nutrition

    • Attain maximal cognitive, motor and sensory function

    • Avoid fever:

      • A proper dressing with antiseptics and cleaning

• MAP: 

• MAP formula = (Systole + 2 x Diastole)/3

  • 70-150:

    • Brain is perfused

•   Cerebral perfusion pressure must be maintained

• Care:

  • Administration of O₂

  • Head of bed elevated by 30 degrees with side-lying:

    • Due to N/V can cause aspiration

  • No NGT or suction:

    • Due to potential leak of CSF and tube can go to brain tissue and increase ICP

  • Prepare for surgery

  • Watch for sodium, sugar, and O2 levels

Head injury health promotion

• Prevent car and motorcycle accidents

• Promote driver safety:

  • Wear safety helmets 

  • Use seat belts and child car seats

  • Do not drive under the influence of drugs or alcohol: Or when you are sleepy (snooze snooze 😪)

    • Do not text and drive or engage in risk-taking behaviors 

• Home safety to prevent fall

Cerebral Edema

• Increased extravascular fluid in brain:

  • Increases ICP

• Variety of causes:

  • Brain tumors

  • Head injuries

  • Infection

  • Stroke

  • Toxic/metabolic issues

Vasogenic Cerebral Edema

• Fluid leaks into the brain's extracellular space due to a compromised blood-brain barrier:

  • Fluids leaks from intravascular to extravascular space:

    • Cleavage of large molecules from capillaries into extracellular space:

    • Increases permeability of blood brain barrier:

      • Fluid in extracellular space:

      • Speed/extent to which the fluid accumulates is influenced by patient:

        • Blood pressure

        • Site of injury

        • Extent of issue with blood brain barrier 

• Most common type

• Occurs mainly in white matter

• Variety of causes

• Continuum of symptoms:

  • Patient can have just headache at first

  • Patient can have focal issues:

    • Difficulty:

      • Speaking

      • Swallowing

Cytotoxic Cerebral Edema

• Brain cells swell from fluid buildup inside them due to cell injury or lack of oxygen.

Interstitial Cerebral Edema

Excess cerebrospinal fluid accumulates around the brain's ventricles due to increased CSF pressure.