Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA)

• DKA results from a relative or absolute insulin deficiency.
• DKA is characterized by:
  • Acidosis
  • Ketosis, where the body uses ketones as its primary energy source
  • Hyperglycemia
  • Dehydration
• DKA mostly occurs in type 1 diabetics because their bodies cannot produce insulin.
• Type 2 diabetics are less likely to develop DKA because their bodies produce insulin, but they may have insulin resistance.
• DKA precipitating factors can include:
  • Illness or infection, such as fever or GI illness
  • Undiagnosed diabetes
  • Inadequate insulin dosage or pump malfunction
  • Noncompliance
  • Changes in diet or exercise, alterations to insulin orders, and being NPO before surgery
• In DKA, the body doesn't make enough insulin, leading to fatty acids converting into ketones and metabolic acidosis.
• Potassium shifts from inside to outside cells, causing an initial high potassium level that decreases with diuresis.
• Important: Hyperkalemia in DKA patients is typically not treated initially because it resolves with treatment.
• Pathophysiology of DKA involves:
  • Lack of insulin
    • Increased blood glucose
    • Tissue starvation
  • Liver converting glycogen into glucose
    • increased blood glucose levels
    • Urinary excretion of glucose
  • Electrolyte imbalance
    • Osmotic diuresis
    • Ketosis
• DKA leads to liver turning glycogen to glucose (ketones), triggering osmosis, which leads to fluid shift and ketones and glucose excretion in urine, resulting in dehydration.
• Severe electrolyte depletion can occur, leading to hypovolemia, shock, worsened acidosis, coma, and death.
• Clinical manifestations of DKA include dehydration exhibited by:
  • Thirst
  • Warm, flushed, dry skin
  • Poor skin turgor
  • Dry mucous membranes
  • Weakness
  • Rapid, weak pulse
  • Hypotension
• Metabolic acidosis can result in:
  • Nausea and vomiting
  • Abdominal pain due to impaired motility and dehydration
  • Sweet, fruity breath
  • Lethargy
  • Coma
  • Kussmaul respirations, characterized by rapid, deep breathing to expel carbon dioxide
  • Polyuria and polydipsia
• DKA testing findings:
  • Serum glucose levels exceeding 250 mg/dL
  • Arterial blood pH below 7.30
  • Serum bicarbonate level below 16 mEq/L
  • Ketones present in urine and serum
  • Anion gap exceeding 10
  • Electrolyte deficits
• DKA interprofessional care:
  • Maintain cardiac monitoring due to the risk of cardiac problems from potassium imbalances; peaked T waves may be present with high potassium.
  • Closely monitor vitals, blood pressure, urine output, and administer oxygen if needed.
  • Administer insulin via SQ or IV infusion.
  • Provide electrolyte replacement.
  • Check blood sugar every hour, or as directed by protocol.
  • The rate of insulin administration is based on the current blood sugar level and its rate of change.
  • Administer 0.45% or 0.9% NaCl IV fluids, usually 500-1000 ml bolus
  • Goal urine output of 30-60 ml/hour.
  • Add dextrose (D5 ½ NS) when blood sugar reaches around 250 to avoid dropping blood sugar too quickly to avoid causing cerebral edema
  • Increase insulin to remove ketones

Hyperosmolar Hyperglycemia Syndrome (HHS)

• It's a life-threatening complication, less common than DKA.
• It results from relative insulin deficiency and is associated with type 2 diabetes.
• Characterized by serum hyperosmolality, hyperglycemia, and altered LOC.
• HHS develops over days.
• Those affected can produce enough insulin to prevent DKA, but not enough to prevent hyperglycemia.
• Patients' blood sugars are typically much higher than those with DKA.
• Common in type 2 diabetics, especially those 60 years and older.
• Pathophysiology involves high blood sugar levels leading to osmotic diuresis, severe dehydration, and electrolyte imbalances.
• HHS manifestations include:
  • Increased serum osmolality
  • Severe dehydration
    • Dry skin and mucous membranes
    • Extreme thirst
    • Altered LOC
    • Polyuria
    • Seizures due to dehydration and elevated glucose
• Common HHS causes are:
  • UTI
  • Sepsis
  • Acute illness
  • Newly diagnosed type 2 diabetes
  • Impaired thirst sensation or inability to replace fluids
• HHS testing typically reveals:
  • Serum glucose above 600 mg/dL, often exceeding 1000
  • Serum osmolality over 320
  • High serum sodium
  • Low serum potassium
• HHS interprofessional care involves similar interventions as for DKA, but necessitates higher volumes of fluids.
• Monitor patients on a cardiac monitor, monitor intake and output, and monitor for fluid overload.
• Priority treatment is massive fluid replacement and determining the cause.
• HHS is a medical emergency with a high mortality rate.
• HHS vs DKA:
  • DKA:
    • Rapid onset
    • Acidosis is a key feature
    • Fruity breath
    • Respiratory manifestations
    • Glucose levels generally lower than HHS
  • HHS:
    • Slower onset
    • Acidosis isn't as likely
    • No fruity breath due to lack of acidosis
    • Respirations not as rapid
    • Glucose levels generally higher than DKA
    • Osmolarity increased due to increased glucose levels
• Both DKA and HHS require cardiac monitoring, intake and output monitoring, and monitoring for fluid overload.

Thyroid Dysfunction: Myxedema

• Severe, long-standing hypothyroidism alters physical appearance with:
  • Puffiness
  • Facial and periorbital edema
  • Mask-like affect (reduced emotional expression)
• Myxedema Coma:
  • Life-threatening complication of poorly managed hypothyroidism or stressors, resulting in a high mortality rate
  • Older adults at higher risk because symptoms can mimic aging.
  • Causes include infection, drugs (especially post-surgical), cold exposure, and trauma.
  • Manifestations: reduced bodily functions
    • Hypothermia
    • Hypotension
    • Hypoventilation
    • Hypoglycemia
    • Hyponatremia
    • Lactic acidosis
    • Cardiovascular collapse
    • Unconsciousness

Myxedema Coma: Interprofessional Care

• Maintain a patent airway due to high aspiration risk.
• Cardiac monitoring
• Perform neuro assessments
• Measure vitals every hour until the patient stabilizes.
• Administer IV fluids and levothyroxine (IV) as the first-line treatment.
• Increase intake and output monitoring, decrease daily weights.
• Perform laboratory tests and treatment, addressing hypoglycemia and low sodium, also ABGs.
• Administer corticosteroids
• Find the trigger and treat it.

Thyroid Storm/Crisis

• Thyroid Storm is a life-threatening state of hyperthyroidism and is very rare.
• It is due to a sudden excess of thyroid hormones, causing a greatly increased metabolism.
• Stressors include infection, trauma, emotional distress, DKA, dig toxicity, uncontrolled hyperthyroidism (Graves disease) and surgery (Thyroidectomy).
• Key manifestations include:
  • Hyperthermia of 106°F (Aspirin is contraindicated)
  • Hypertension
  • Tachycardia/Palpitations
  • Dyspnea
  • Heart failure
  • Shock
  • Abdominal pain, vomiting, and diarrhea
  • Agitation, confusion, psychosis, delirium, seizures, and coma
• Treatment: Medication regimen to reduce TH (Thyroid Hormone) synthesis and secretion.
  • Examples are antithyroid medication like Tapazole, sodium iodine (administered 1 hour after Tapazole), and propanol to block SNS effects.
• Nursing interventions for thyroid storm/crisis are:
  • Cooling measures
  • Replacing fluids, glucose, and electrolytes
  • Administering oxygen
  • Stabilizing the heart

Addisonian Crisis

• Addisonian crisis involves an acute, life-threatening response to adrenal insufficiency.
• Triggers include stress, adrenal surgery, sudden pituitary gland destruction, or sudden withdrawal of corticosteroid therapy.
• Decreased aldosterone leads to increased potassium levels.
• Decreased cortisol causes decreased gastric motility, decreased blood sugar, increased calcium and BUN.
• Manifestations involve:
  • High fever
  • Weakness
  • Confusion
  • Severe abdominal pain
  • Low back and leg pain
  • Severe vomiting and diarrhea
  • Hypotension that can lead to shock.
  • Tachycardia
  • Dehydration
  • Electrolyte imbalances: hyperkalemia, hyponatremia, hypoglycemia.
• Treatment includes:
  • Rapid IV fluid with normal saline or dextrose, glucocorticoid replacement via high doses of hydrocortisone.
  • Electrolyte replacement.

Addisonian Crisis: Nursing interventions

• Assess vitals and neurological status.
• Monitor electrolytes and fluid overload.
• Avoid stressors and treat underlying triggers.
• Teach patients regarding adjusting corticosteroid doses during planned stress.
• All patients should carry 100 mg of IM hydrocortisone for emergencies.

Intracranial Pressure (ICP)

• ICP results from a balance between brain tissue, blood, and cerebrospinal fluid (CSF).
• Key factors influencing ICP are:
  • Arterial and venous pressure, which impacts MAP (mean arterial pressure)
  • Intra-abdominal and intrathoracic pressure
  • Posture (patients should be at least 30 degrees and midline for optimal CSF drainage)
  • Temperature
  • Blood gases, particularly managing CO2 levels to prevent vasodilation
• Normal ICP is less than 15 mmHg, values over 20 mmHg are cause for concern.
• Cerebral Blood Flow requires autoregulation, is regulated based on the body, and sufficient cerebral perfusion pressure
• CPP (cerebral perfusion pressure) = MAP - ICP; normal CPP is 60-80 mmHg, and below 50 results in ischemia.
• Factors that affect cerebral blood flow include carbon dioxide, hydrogen ions, tumors, bleeding, and stroke.
• Progression of increased ICP:
  • Can be life-threatening
  • Elevated pressure will distort brain tissue and cause neurological deficits and hypoxia.
  • Sustained pressure can depress the brain stem, leading to herniation or respiratory arrest

Cerebral Edema

• It causes increased ICP.
• It is an accumulation of fluid in the brain.
• Vasogenic edema: most common, in white matter.
• Cytotoxic edema: results from destructive lesions or trauma.
• Interstitial edema: typically due to excessive CSF production linked with hydrocephalus.
• Clinical manifestations:
  • Decreased LOC
  • Vitals changes
  • Motor function impairment
  • Eye issues headache and nausea/vomiting

ICP Monitoring and Management

• ICP measured via ventricles, the subarachnoid, subdural, or epidural spaces, using a pressure transducer
• Gold standard tool utilizes ventriculostomy.
• Nursing Considerations:
  • Level transducer with the tragus of the ear.
  • Must be zeroed with each patient repositioning.
  • Monitor for pressure on the monitor.
  • Try to use for no longer than 5 days.
  • Normal CSF production is 20-30 mL/hour.
  • Never perform lumbar puncture with neurological problems
• LICOX Catheter: measures oxygenation and temperature in the brain's white matter (preferred temp = 96.8°F).
• Increased ICP impacts motor function, including:
  • Contralateral hemiparesis/hemiplegia (opposite side weakness or paralysis)
  • Decerebrate (extensor) posturing, more serious damage
  • Decorticate (flexor) posturing.
• Additional signs of increased ICP:
  • Continuous headaches, which worsen in the morning; can signal tumors or lesions
  • Vomiting (unexpected and projectile)
  • Changes in LOC (most reliable indicator)
  • Pupil changes
  • Vision Loss, Double Vision
  • Compression of Cranial Nerves
  • Papilledema
  • Sensory/Motor Function Loss
  • Cushing Triad
• Nursing assessment involves:
  • Monitoring for lack of perfusion and dysrhythmias
  • Managing airway, breathing, and circulation, watching vitals, and being aware that respiratory changes are associated with high ICP
  • Complete Neurological Assessment

Methods to Decrease ICP

• Elevate the head of the bed to improve cerebral venous outflow
• Oxygenation and ventilation support.
• Monitor ICP via CSF drainage
• Monitor vital signs
• Don't suction every 2 hours; monitor ABGs, may need NG tube
• Create a Quiet environment
• Prevent injury and initiate seizure precautions
• Administer Osmotic/Diuretic Drugs
• Administer Antipyretic
• Administer Anticonvulsant

Medications

• Administer Mannitol
• Administer Hypertonic Saline (3%)
• Administer Corticosteroids unless TBI

Drug Therapy

• Mannitol reduces brain pressure by reducing CSF production
• Hypertonic saline solution (3% saline) increases serum sodium levels and can be a first-line agent for symptomatic cerebral edema with low sodium.
• Monitor fluid and electrolyte balance.
• Corticosteroids are used for swelling in the brain, but not for TBI (traumatic brain injury).
• Antipyretics (Tylenol) are used to manage fever and prevent shivering.
• Barbiturates can help with increased ICP but only in high doses when other drugs are not working.
• Antiseizure medications are also used.

Nutritional Therapy

• Ensure the patients are hypermetabolic and hypercatabolic
• Utilize Entral and Parenteral Nuitrition
• Provide early feeding
• Monitor fluid and electrolyte volume

Head Trauma

• Diffuse Axonal Injury involves widespread axonal damage in mild, moderate, or severe TBI with decreased LOC.
• Epidural Hematoma requires rapid treatment! Can result in venous or arterial origin and increase ICP

Head Trauma Hematoma

• Classic signs of Epidural Hematoma:
  • Brief Loss of Conciousness
  • HA
  • N/V
  • Neuro Emergency

Subdural Hematoma

• Signs/Symptoms can present weeks after initial injury
• Pt. may also have seizures

Intracerebral Hemorrhage

• Size and location of hematoma are critical key to determine pt. outcome
• Prevent secondary Injury through interprofessional care.
• Vascular Injuries can cause increase ICP and Swelling

Always Neuro Check

• Assess pupils

Stroke - Pathophysiology

• The Carotid and Vertebral arteries supply blood to the brain
• Stroke means reduced blood flow to to artery is reduced by clot or rupture leading to reduction in glucose and oxygen supply to the brain
• Reduced flood flow results altered neurological metabolosim in 30 sec
• Stroke = Brain Damage!
• Irreversible cell damage in 5 minutes!

Risk Factors

• Modifiable include obseisty, diet, exercise, smoking, HTN
• Non-Modifiable include the age (stroke risk doubles each decade after 55)
• Ischemic Stroke results from inadequate blood flow to the brain tissue

Signs and Symptoms of Stroke

• Decreased level of conciousness
• Hemotoma
• Often proceeded by TIA
• Can be due to embolisms or thrombosis
• Stroke can also result in Hemorrhage and occurs when an embolus lodges in and occludes a cerebral artery. *Bleeding!
• *Hemorrhage
• Hypertension main cause
• Neurological deficits that result in deviation of the eyes, headache, nausea and vomiting as well

Subarachnoid Hemorrhage (SAH)

• Intracranial Bleeding caused by ruptured aneurysm (trauma)

• Called the "Silent Killer"

• The majority of aneurysms are in the circle of Willis
• Calcium Chanel Blockers (CCB) are provided for brain protect! and are given WITH SAH

Nursing Interventions

• Ensure proper diagnosis, blood flow and treat increased ICP!

Stroke - Diagnosis

• Primary Diagnostic TEst = Non Contrast CT (*Without Contrast!)

Interprofessional Care

• The #1 thing to remember is Time of Onset of Strokes is Key!
• Need to know when signs and symptoms have started
• Key Signs to remember and Act FAST!
  • Fast (facial drooping, arm weakness, speech impairment, time)
• Prioritize ABCs! *Airway, Breathing, Circulation
• Stroke Assessment done with NIH
• HTN common immediately after a stroke
• Depending on the Type of Stroke treat HTN differently
  • ISCHEMIC STROKES
  • DO NOT treat HTN if <220/120 as long as elevated BP helps prevent Ischemic Zones that become infarcted!
  • However - always monitor blood glucose levels, and electrolyte function

Drug Therapy

• VERY Important to KNOW THESE Drugs!*
• Fibrolytic therapy IV to reestablish BF in acute symptoms!
• Needs to be administered in 3-4.5 hours!

Treatment

• Ballon Catheters to insert Stent and keep Artery Open
• Hemorrhagic Strokes result from too much bleeding!

Emergency Management

• The most important question you can ask a pt that presents in emergency:
• -When did all this start?*
  • Be able to assess -Alterations in Levels of Conciousness -Difficulty Swallowing

End of Life (Brain Death)

-The most important test used to determine brain death: -Oculocephalic Brain Death (When moving a pt side to side they will hold pt eyes up to make sure they don't move)

• If there is no breathing for 10 minutes will pronounced brain dead.
• Deceased donation is donating body/organs after someones death
• KODA is an organ donation org
  • KODA will be contacted on every pt. with death.

The Organs in Need (Kidney, Heart, Liver, Lungs, Panceras, Small Intestine!)

• KODA Maintained Fluid, Volume, and Circulation so always continue to monitor their airway!

Subjective Evaluation

• Evaluate the G1 (Gastrointestinal) track functions through various methods.

Cirrhosis

• Alcohol main cause!
  • Damages Liver

Diagnostics:

-Remember ALT AST

• Main Enzyme type.
• Alkaline levels also used for testing Low Cholesterol

Treatment

• Lactolose and remove the GI
• LiverTransplant is very important to treating.

Acute Pancreatitis

• Inflimation of the Pancreas due to autodigesting of Pancreatic Enzymes
• Sudden with Diabetes and Shock
• Sudden, severe acute pancreatitis causes massive hemorraging and destruction of pancreas that can lead to acidosis *

Assessment is "ELevated Serum Levels and Amalayse (ESLA)"

• High elevated serum lipase and aminoase + High
• ERCP are used and obtained in high endoscpeys
• Many can experience elevated levels due to pancreatitis:
• Elevated Liver Enzymes, Glucose and Potassium ect. -Remember Electrolyte Volume - High volume to treat pancreatitis
• *Important to be remembered is Demerol(Dilaudid - pain is A No GO!)
• Should be avoided in pt. with paralytics

Nutritional Therapy

NPO -

• Low Fat!*
• High Card Diets are important to remember*

G-B

• Pt. must be able to do enteral/parenteral therapy
• Know what's not clean and what needs to be sanitized!
• Remember to wear a mask!

Explore diabetic ketoacidosis (DKA), characterized by acidosis, ketosis, hyperglycemia, and dehydration, often due to insulin deficiency. Learn about the causes, including illness/infection, undiagnosed diabetes, inadequate insulin dosage and potassium shifts in DKA. Mostly affects type 1 diabetics.