Diabetic Ketoacidosis (DKA)

• Study notes are generated based on the information provided in the text
• Focus is on comprehension and knowledge retention

Diabetic Ketoacidosis (DKA)

• DKA is a state of relative or absolute insulin deficiency.
• It is characterized by acidosis, ketosis, hyperglycemia, and dehydration.
• Ketosis is a hallmark, in which the body uses ketones as the primary energy source instead of glucose.
• Type 1 diabetics are more prone to DKA because their bodies do not produce insulin.
• Type 2 diabetics produce insulin but cannot use it effectively due to insulin resistance, making them less likely to develop DKA.

DKA: Precipitating Factors

• Illness or infection, especially fever or GI illness
• Undiagnosed diabetes
• Inadequate insulin dosage or pump malfunction
• Noncompliance with insulin regimen
• Changes in diet or exercise, insulin order, and NPO status before surgery

DKA Pathophysiology

• Insufficient insulin leads to rapid fatty acid development and conversion into ketones.
• Ketones contribute to metabolic acidosis.
• Potassium shifts from intracellular to extracellular spaces, potentially causing initial hyperkalemia that resolves with diuresis.
• Liver converts glycogen to glucose and releases it into the bloodstream
• Osmosis is triggered, leading to fluid shift
• Glucose and ketones in urine cause dehydration.
• Severe electrolyte depletion (sodium, potassium, chloride, magnesium, phosphate) can lead to hypovolemia, shock, worsened acidosis, coma, and death.

DKA: Overview of Pathophysiology

• Lack of insulin
  • Increased blood glucose levels
  • Tissues starved for energy
• Liver converts glycogen to glucose
  • Blood glucose levels increase
  • Glucose excreted in the urine
• Electrolyte imbalance
  • Osmotic diuresis
  • Ketosis

DKA: Clinical Manifestations

• Dehydration: thirst, warm/flushed/dry skin, poor turgor, dry mucous membranes
• Weakness
• Rapid, weak pulse
• Hypotension
• Metabolic acidosis: nausea, vomiting, abdominal pain (impaired motility/dehydration)
• Hallmark: sweet, fruity breath
• Lethargy, coma
• Hallmark: Kussmaul's respirations (rapid, deep breathing to eliminate carbon dioxide)
• Polyuria, polydipsia

DKA Testing and Findings

• Serum Glucose: Greater than 250 mg/dL
• Arterial Blood pH: Less than 7.30
• Serum Bicarbonate Level: Less than 16 mEq/L
• Ketones: Present in urine and serum
• Anion Gap: Greater than 10
• Electrolytes: Deficits
• Anion Gap: Positive electrolytes, ketones
• Serum Osmolality: High (water and electrolyte imbalance)

DKA Interprofessional Care

• Oral Fluids: Encouraged
• IV Fluids:
  • 0.45% or 0.9% NaCl: 500-1000 mL bolus.
  • Goal: urine output 30-60 mL/hour.
  • Add dextrose (D5 ½ NS) when blood sugar around 250 to avoid rapid blood sugar decrease (cerebral edema).
• Remove ketones by increasing insulin
• Fluids address metabolic acidosis
• Risk of cardiac problems due to potassium levels, so cardiac monitoring is essential.

Additional DKA Considerations

• Cardiac monitoring
• Possible peaked T waves if potassium is high.
• Monitor vitals, BP, and urine output.
• Administer oxygen as needed.
• Insulin administration
  • Subcutaneous or IV infusion.
• Electrolyte replacement as needed.
• Check blood sugar hourly.
• Rate of administration based on current and previous blood sugar levels/changes.

Hyperosmolar Hyperglycemia Syndrome (HHS)

• Life-threatening, less common than DKA.
• Relative insulin deficiency
• Typically Type 2 diabetics
• Characterized by serum hyperosmolality, hyperglycemia, and altered level of consciousness.
• Develops over days.
• Patients produce enough insulin to prevent DKA but not hyperglycemia.
• Blood sugars are extremely high
• Occurs in Type 2 diabetics, 60 years and older.
• High glucose levels cause polyuria and dehydration.

HHS Pathophysiology

• Patients have very high blood sugar and the body attempts to fix it via osmotic diuresis.
• Leads to fluid deficit and electrolyte imbalances.
• Patients are severely dehydrated.

HHS: Manifestations

• Increased serum osmolality
• Severe dehydration: dry skin/mucous membranes, extreme thirst
• Altered level of consciousness
• Polyuria
• Seizures due to dehydration and elevated glucose

HHS: Common Causes

• UTI
• Sepsis
• Acute Illness
• Previously undiagnosed Type 2 diabetes
• Impaired thirst or inability to rehydrate

HHS Testing

• Serum glucose levels >600 mg/dL, and often >1000 mg/dL
• Osmolality >320
• Serum Na+ High
• Serum K+ Low

HHS Interprofessional Care

• Medical Emergency with high mortality rate
• Similar to DKA
• Correct fluid and electrolyte imbalances.
• Patients need larger volumes of fluid
• Administer IV fluids and IV insulin.
• Correct the underlying cause.
• Cardiac monitor, strict I&O monitoring.
• Prioritize rapid, massive fluid replacement to treat these patients.

DKA vs HHS

• DKA: Rapid Onset

• Acidosis is seen

• Fruity Breath

• Respiratory Manifestations

• Glucose is generally lower in comparison to HHS

• HHS: Slower Onset

  • Acidosis is less likely
  • No fruity breath
  • Respirations are not as rapid
  • Glucose is generally higher
  • Osmolarity is increased due to the increased Glucose

• Both require a cardiac monitor, and strict I&O, with close attention on fluid overload

Thyroid Dysfunction: Myxedema

• Severe, long-standing hypothyroidism.
• Alters physical appearance of the skin and subcutaneous tissue: puffiness, facial/periorbital edema, mask-like affect (lack of emotion).
• Older adults at risk as symptoms mimic aging.

Myxedema Coma

• Life-threatening complication of untreated/poorly managed hypothyroidism or stressors; high mortality rate

Myxedema: Causes

• Infection, drugs (post-surgical patients), exposure to cold/trauma

Myxedema: Manifestations

• LOW
  • Hypothermia, hypotension, hypoventilation, hypoglycemia, hyponatremia, lactic acidosis, cardiovascular collapse, unconsciousness/coma

Myxedema: Interprofessional Care

• Maintain patent airway, because these patients are at high risk for aspiration
• Cardiac monitoring/Neuro assessment
• Vitals (BP/temp) every HOUR until patient stabilizes
• Administer IV fluids and levothyroxine IV (first line of treatment)
• Increase I&Os should, decrease daily weights
• Treat hypoglycemia/hyponatremia, ABGs and corticosteroids
• Find and treat trigger.

Thyroid Storm/Crisis

• Extreme state of hyperthyroidism (life-threatening), rare.
• Sudden surge of thyroid hormones, increasing metabolism significantly
• Stressors: infection, trauma, emotional stress, DKA, dig toxicity, uncontrolled hyperthyroidism (Graves disease), surgery (thyroidectomy)

Thyroid Storm/Crisis: Manifestations

• Fever, even as high as 106, do not give ASA
• Hypertension/Tachycardia/palpitations
• Dyspnea/Heart failure
• Shock
• Abdominal pain, vomiting, diarrhea
• Agitation, confusion, psychosis, delirium, seizures, coma

Thyroid Storm/Crisis: Intervention

• Medication regimen to reduce TH synthesis and secretion
• Antithyroid medication: Tapazole
• Sodium iodine (1 hour after Tapazole)
• Propanol (to block SNS effects)
• Interprofessional care
• Cooling measures
• Replacing fluids, glucose, and electrolytes
• Administering oxygen Stabilizing heart

Addisonian Crisis

• Life-threatening response to adrenal insufficiency

Addisonian Crisis: Triggers

• Stress
• Adrenal surgery
• Sudden pituitary gland destruction
• Sudden withdrawal of corticosteroid hormone therapy
• Decreased aldosterone (mineralocorticoid) leads to increased potassium.
• Decreased cortisol (glucocorticoid) includes decreased gastric motility(decreased BS), increased calcium and BUN.

Addisonian Crisis: Manifestations

• High fever
• Weakness/Confusion
• Severe abdominal, low back, and leg pain
• Severe vomiting and diarrhea
• Hypotension leading to shock
• Tachycardia/Dehydration
• Electrolyte imbalance: hyperkalemia, hyponatremia, and hypoglycemia

Addisonian Crisis: Interprofessional Care

• Rapid IV fluid administration: NS/Dextrose
• Glucocorticoid replacement: high doses of hydrocortisone
• Electrolyte replacement is needed
• Assess vitals and neuro status.
• Monitor electrolytes and for fluid overload
• Avoid stressors/Treat underlying trigger
• Patient education key on how to adjust corticoid steroids with planned stress
• Pt should carry 100 mg of IM hydrocortisone with them in emergency.

Intracranial Pressure (ICP)

• Balance between brain tissue, blood, and cerebral spinal fluid (CSF)

Factors Influencing ICP

• Arterial Pressure/Venous Pressure, can affect MAP
• Intraabdominal and intrathoracic pressure
• Posture- Head of bed at least 30 degrees and midline to allow CSF to drain

ICP Influenced By

• Temperature
• CO2 levels
  • High levels can cause vasodiation

ICP Norms And Cerebral Blood Flow (CBF)

• Normal to find less than 15 mm Hg.
  • Anything sustained above 20 is abnormal
• Cerebral autoregulation that regulates blood flow in response to change
• Cerebral Perfusion Pressure (CPP)
  • Pressure needed to ensure blood flow to the brain
  • CPP equals MAP - ICP

CPP Norms And Factors Affecting CBF

• Normal CPP is 60-80 mmHg.
  • Below 50 is associated with ischemia
• Factors include CO2, hydrogen, Tumors, Stroke, Etc.
  • These can cause bleeding, swelling and or decreased oxygen is decreased

Progression Of ICP

• Could be life-threatening; result of increase in any or all of 3 components in the brain: CSF, blood, brain tissue.
• As ICP elevates edema will distort the brain tissue, will see neuro deficits and tissue hypoxia due to patient usually becoming acidic
• If ICP is sustained brain stem comes depressed and eventually it herniates leading to respiratory arrest and brain death

Herniation & Cerebral Edema

• Herniation requires a normal head, uncal, central, subfalcine and clarivial
• Cerebral Edema
  • Causes an Increase in ICP
  • Increased accumulation of fluid in the extravascular spaces of the brain tissue
• Three types of cerebral edema:
  • Vasogenic: most common in white matter
  • Cytotoxic: caused by destructive lesions or trauma
  • Interstitial: fluid in the brain due to excessive CSF production
    • Think Hydrocephalus

Decreased LOC, ICP Nursing Considerations

• Decreased LOC, changes in vitals, motor function, eyes, H/A, N/V
• Can measure in the ventricles; uses pressure transducer
• Gold standard is monitoring is ventriculostomy
• Tragus of the ear used to level the transducer to formina of M using the same location every time
• Monitor pressure every time patient is moved
• Normal CSF production is 20-30 mL/Hour
• NEVER do a lumbar puncture is someone already exhibits a neuro problem

Headaches, Vomiting, Assessment For ICP

• Headache
• continuous, and worse in the morning, tumor concerned
• Vomiting
• Not preceded by nausea
• Projectile Clinical Manifestations
• Change in LOC.
• H/A
• Pupillary changes
• If they are fixed and dilated they probably already herniated
• Compression of cranial nerves
  • Can see sluggish and non-responsive pupils
• Papilledema

Cushing Triad & Interventions For ICP

• Cushing Triad: widening pulse pressure, altered respiration, bradycardia
• Monitor for lack of perfusion & dysrhythmias
• Check ABC's/ Vitals
• Changes in respiration can signal high ICP
• Neurological signs are important to check
• Glasgow Coma Scale (GCS): if 8 or less- coma ; check GAG reflex

ICP & Interprofessional Care

• Interventions include giving patient a quiet/calm environment
• Methods to decrease ICP include raising the head of the bed with patient midline
• Perform Oxygenation/Ventilation and monitor CSF
• Prevent injury or seizures
• Drug Therapy- continue to monitor FVE
• Mannitol will decrease production of CSF, be sure to monitor electrolytes
• Use Hypertonic solutions to draw fluid from patient with edema
• DO NOT use corticosteroids for patients with TBI, be sure to monitor blood levels!

Head Trauma

• Antipyretics are use to cool due to not wanting patient shivering
• Nutritional: early feeding is important for increased success
• Injuries involve widespread axonal damage by TBI that can be moderate or severe
• Can have increased ICP and decerebration due to brainstem damage
• Basilar skill fracture happens at base of skull
  • Can include a tear in the dura where fluid leaks

Head Injuries, Contusions, Hematomas

• Check for Cerebral Spinal Fluid (CSF) in Halo sign
• Epidural Hematoma (Bleed between brain and skull)
• Venous emergencies can cause an arterial bleed quickly with classic signs of unconsciousness followed by lucidity
• Subdural bleeds can cause complain of headaches without signs and symptoms until later
• Size and location key to determining patient outcome

Vascular & Head Injuries

• Prevent them when administering interprofessional care
• Monitor for symptoms, treat any issues that develop
• Assessments are timely with CT scans, MRI, always check pupils

Stroke: Pathophysiology & Modifiable Risk Factors

• Supplied to the artery by carotid & vertebral arteries
• Ruptures or blockages can decrease flow
• Severely altered if neurological metabolism is stopped in 2 minutes
• Regardless of hemorrhagic or ischemic injuries can effect functionality
• Modifiable risks: obesity, diet, exercise, smoking, diabetes, HTN

Stroke: Non-Modifiable Risk Factors

• Age (stroke risk doubles each decade after 55), gender (men are more likely than women), race (black more likely than white)
• Ischemic and thrombolytic strokes occur with total or partial occlusions in the brain which prevent tissues from receiving fuel to the brain

Ischemic Stroke: Symptoms

• Will not see decreased LOC within first 24 hours but may see changes caused by edema that can proceed TIA
• Thrombosis: result of narrowing of blood vessel often occurred in patient with HTN
• Embolic: results in rapid infection due to edema caused by A-fib

Hemorrhagic Stroke

• Results from bleeding into the brain that can be life threating due to rapid complications

Stroke: Diagnostic Studies & Interventions

• W/out contrast is test performed to rule out hemorrhage as a result to ischemic, should start the w/o first
• When symptoms of a stroke occur always perform a study ASAP
• Ischemic
• Balloon catheter is use to help place stent
• Carotid Enerectomy remove blood build up
• Hemorragic:
• Drug:
• Anticoagulation
• Seizure prophlaxis

Stroke: Anerysms

• Commonly cause by rupture, cause a Cerebral aneuryism can result by trauma/ illicit drug use as a " silent killer"
• In effort to protect with calcium channel blocker to increase calcium levels
• Always make sure to elevate bed 30 degrees

Brain Death

• Is when the patient swells due to decreased oxygen supply causing brain tissue dies
• Test are preformed to confirm this Brain injuries result from the body function

KODA & Brain Injuries

• Medical staff are require to call on every death regardless of age
  • KODA representative check the stern checklist when okaying death
  • Has types of donation; tissue, organs
• Hemodynamic stability must be sustain, with vitals, output map ranging betweem 60-100

Abdominal Assessments: Subjective & Objective

• GI system is access in case their are any related concerns

Abdominal Assesments & Aging Factors

• Factors show the patients potential of disteress, decrease of empyting of protein

Cirrhosis

• Chronic progressive disease of the liver, is irreversiable with 2x more in men

Cirrhosis: Treatment, Diagnoses

• Alcohol leading, will need blood, is checked

Cirrohosis: Complications

• Increased ast, albumin

Ascites

• Ascities are due to 3rd space
• Decreased albumin can be caused in multiple ways

Ascites: Management & Nursing interventions

• Care is to assist
• Treatment can also to draw fluids

Esophogeal Gastric Varices

• Causes the smaller vessels to distin, but the tissue to easily bleed

Esophogeal Gastric Varices: Managaement & Treatment

• Stabilize during the Drug:

KODA & Treatment of Liver/ Brain Injuries

Treatment may also prevent clotting with many things

This lesson covers diabetic ketoacidosis (DKA), a state of insulin deficiency characterized by acidosis, ketosis, hyperglycemia, and dehydration. It outlines precipitating factors such as illness, undiagnosed diabetes, inadequate insulin dosage, and noncompliance. Also explores the pathophysiology of DKA, including rapid fatty acid development and conversion into ketones.