Critical Care Finals Study Guide

1.Hyperkalemia: Treatment: ● Acute hyperkalemia can be treated temporarily by emergent IV administration of insulin and glucose. ● Extreme hyperkalemia can be acutely manage with IV insulin and glucose must be administered at the same time to avoid hypoglycemia as secondary complication ● K is permanently removed from the bloodstream by cation-exchange resin products such as sodium polystyrene sulfonate (Kayexalate), placed into the GI tract or is removed directly from the blood by hemodialysis. Monitoring: (>4.5 mEq/L) CF: Irritability and restlessness, anxiety, nausea and vomiting, abdominal cramps, weakness, numbness and tingling (fingertips and circumoral), and Cardiac irregularities. Pathology behind treatment: Forces potassium out of the serum and into the cells. 2.Trauma: Treatment: ● Golden hour a critical time frame; Activation of EMS, stabilization and transport, triage, initial resuscitation, early surgical consultation, and provision of critical care ● Airway maintenance ● Recognition and control of external bleeding and shock ● Immobilization of the patient are essential priorities ● ABCDEs of trauma resuscitation; Airway, breathing, circulation, disability, and exposure Complications of treatment: ● Infection, sepsis, transfusion-related complications (fever, hypoxemia, and hypotension), missed injury, multiple organ dysfunction syndrome 3.Heart failure: Treatment (including types of medications): ● Ace inhibitors to inhibit LV remodeling and dilation. If not tolerated ARBs (Losartan) may be used ● Low dosage of beta blockers (carvedilol) - strict surveillance to avoid untoward negative inotropic effects ● Digoxin ● Cardiac resynchronization therapy (CRT) ● Diuretics to dec preload ● Morphine for peripheral dilation and dec anxiety ● Nitrates dec preload and vasodilate the arteries ● Positive inotropic meds (dopamine) to inc contractility ● Intra Aortic balloon pump can be temporarily used to dec afterload ● Maintain fluid balance: low sodium diet Complications of treatment: ● Hypotension ● Electrolyte imbalance ● Renal dysfunction 4.Ventricular Tachycardia: Treatment: ● Depends whether the pt is stable or unstable ● Cardiac catheterization ● Electrophysiologic testing ● Antidysrhythmic meds (amiodarone and lidocaine ● Ablation of the reentrant pathway w/n the ventricle ● Inserting an implantable cardioverter defib (ICD) Complications of treatment: ● Conversion to V fib during cardioversion ● Hypotension ● Pulmonary edema due to inc myocardial demand Assessment: ● Pulseless VT is life threatening ● Low BP ● Pt may lose consciousness and needs immediate CPR and defib 5.Valve replacements: Nursing education: ● Risk factor modification to prevent coronary artery dx (smoking cessation, regular exercise, weight loss) ● Post op incisional care ● Activity limitation (no lifting, or pulling anything heavier than 10 lbs for 6-8 weeks) ● Follow up appointment ● Antibiotic prophylaxis before invasive procedures ● Anticipated mood changes after surgery ● Adherence to anticoagulation/ antiplatelet therapy (clopidogrel for those who can’t take aspirin) Post-op care: ● Monitoring of mental stat, telemetry, VS, volume stat, and possible blood work Medication post-op: ● IV beta blockers (esmolol) or CA channel blockers (diltiazem) for tachycardia to slow supraventricular rhythms. ● Crystalloids for fluid resuscitation ● Tx for post op bleeding; Aminocaproic acid (Amicar), Desmopressin acetate, Protamine sulfate ● Vasopressors for hypotension; Norepinephrine and vasopressin ● Inotropic catecholamine to enhance EF; Epinephrine, norepinephrine, dopamine, and dobutamine Medication education/ assessment: ● 12 lead ecg ● Monitor electrolytes ● For pt who cannot take beta blockers, amiodarone is an alternative to reduce the incidence of post op Afib 6.Nitroglycerin: Reasons to give: ● Use to vasodilate the coronary artery and dec pain (angina) ● To relieve angina pectoris (chest pain) Complications: ● Hypotension and headache Nursing assessment: ● Monitor patient for relief of chest pain, for return of ST segment to baseline ● Avoid giving when systolic BP is <90 mmhg ● Do not give when pt is taking Sildenafil or Viagra can cause precipitous fall in BP 7.Diabetes Insipidus: Signs and symptoms: ● Increase urine output (polyuria) occurs in absence of diuretics, a fluid challenge or hyperglycemia ● Central DI due to increase ICP (life threatening) ● Polydipsia (excessive thirst) ● Dehydration ● Hypotension ● Tachycardia Nursing interventions: ● Administration of prescribed fluids and medications (desmopressin) ● Evaluation of response to therapy ● Administer hormone replacement therapy with desmopressin to manage central DI Assessment: ● Monitor BP, HR, CVP and pulmonary artery pressure ● I/O measurement ● Serum sodium (>145 mEq/L), sodium osmolality( >295 mOsm/kg), and urine osmolality (<300 mOsm/kg), urine specific gravity (<1.005) ● Measurement of ADH (1 to 5 pg/mL) ● Copeptin a biomarker for the differential diagnosis of the polyuria polydipsia syndrome ● Assess for signs of dehydration such as dry mucous membranes, dec skin turgor, and orthostatic hypotension ADD: Central DI - synthesis of ADH is incomplete in the hypothalamus - usually caused by neurosurgery, traumatic head injury, tumors, icp, brain death, infections Nephrogenic DI - Congenital or acquired - Vasopressin in kidney tubule is nonresponsive decreasing the responsiveness of kidney tubules to ADH - Long term us of lithium carbonate is a frequent culprit 8.Lumbar puncture: USUALLY BETWEEN L3 TO L4 OR L4 TO L5 Indication: ● Diagnostic tool to evaluate for conditions such as meningitis, subarachnoid hemorrhage, and multiple sclerosis ● CSF analysis for presence of blood or infection in the subarachnoid space ● Placed in flexed lateral recumbent position ● Collection of 30 mL CSF Complications: ● Cerebral herniation including space-occupying lesion with mass effect, ● abnormal intracranial pressure caused by increased CSF pressure ● Arnold-Chiari malformation (brain tissue extends into the spinal canal) ● increased bleeding risk (thrombocytopenia, coagulopathies, anticoagulant meds), ● local infection at the puncture site ● CSF leak (headache)- anesthesia puts a blood patch up? ● CSF look when draining- yellow halo ring with a dot of blood in the middle 9.Pneumothorax: Types: ● Tension pneumothorax(emergent!)- when air enters the pleural space on inhalation and cannot exit on exhalation. ○ Clinical Signs- diminished breath sounds, hyperresonance to percussion, tachycardia, hypotension, sudden chest pain extending to the back, neck, or shoulders. ○ Tracheal deviation (late sign) ○ Tx- Needle decompression- insertion ● ● ● ● of a large bore needle or cath into the 2nd intercostal space at the midclavicular line of the affected side and oxygen administration Open Pneumothorax- occurs as a penetrating chest trauma ○ Subcutaneous emphysema (air trapped in the skin) ○ Tx: promptly inserting a chest tube, if chest tube is not immediately available, covering the wound at end expiration w/ a sterile occlusive dressing taped securely on 3 sides and large enough to overlap the edges of the wound should be used ○ Surgical intervention is required to close the wound Closed- occurs as a result of blunt chest trauma Iatrogenic- occurs as a result of therapeutic or diagnostic procedures, such as central line insertion, thoracentesis, and needle aspiration Massive hemothorax- blunt or penetrating thoracic trauma can cause bleeding into the pleural space ○ Accumulation of more than 1500 mL of blood in the thoracic cavity ○ Assessment findingsdiminished or absent breath sounds over the affected lung and collapsed neck veins (Hypovolemia) or distended neck veins)coexisting tension pneumothorax. ○ Massive hemothorax is diagnosed with the basis of hypovolemia with absence of breath sounds or dullness to percussion on one side of the chest ○ Tx- fluid resuscitation to treat hypovolemic shock. Chest tube is placed on the affected side to allow drainage of blood. Assessment: ● If pneumothorax is large, hypoxemia ensues, and ALF quickly develops. Bulging intercostal muscles, tracheal deviation, hyperresonance with dec or absent breath sounds ● Increased pressure within the chest can lead to shifting of the mediastinum, compression of the great vessels and dec CO. Nursing actions: ● Optimizing oxygenation and ventilation, maintaining chest drainage system, providing comfort and emotional support, and maintaining surveillance for complications. 10. Assessment for brain death Brain death is the irreversible cessation of all brain function. Clinical examination has 3 components: absence of cerebral motor reflex, absence of brainstem reflexes, and absence of respiratory drive ● Cerebral motor responses: stimulation of pain by application of pressure to the nail beds or supraorbital ridge. ● Brainstem reflex: ○ Pupillary reflex- absence of light reflex, dilated pupils may remain after brain death has occurred. ○ Oculocephalic reflex- also called “doll’s eyes”, fast turning of the head to both sides. In brain death this should not generate any eye movement ○ Oculovestibular reflexalso called “cold calorics”. Head of the bed is elevated 30 deg, and approximately 50mL of ice water or normal saline is injected to the ear; no movement of the eye towards the side of the stimulus should be present. Observe pt for up to 1 min after each irrigation and 5 min should be allowed before testing the opposite ear. Meds that can influence this reflex include sedatives,, aminoglycosides, tricyclic antidepressants, anticholinergics, and antiseizure agents. ○ Corneal and jaw reflexespharyngeal and tracheal reflexes are absent in pt with brain death. Evaluate gag reflex by stimulating the posterior part of the pharynx with a tongue blade. Cough reflex can be tested with bronchial suctioning. ● Apnea testing: The loss of brainstem function results in the loss of centrally controlled breathing with resultant apnea. ○ Demonstration of the absence of spontaneous breathing when disconnected to the ventilator ● Meds that can alter these test: Paralytics and sedatives ● Additional confirmatory tests: cerebral angiography, electroencephalography, transcranial doppler, and cerebral scintigraphy. 11. ICP: Complications: ● Decreased blood flow to the brain causing brain damage ● Herniation of intracerebral contents results in the shifting of tissue from one compartment of the brain to another and places pressure on the cerebral vessels and vital function center of the brain, if unchecked , it rapidly causes death. Assessment: ● Changes in LOC most sensitive indication of increase ICP ● GCS, VS ● Unequal pupil size, dec pupillary response to light, headache, projectile vomiting, altered breathing patterns, cushing triad (bradycardia, systolic hypertension, and bradypnea), diminished brainstem reflexes, papilledema, and abnormal extension (decerebrate), or flexion (decorticate) ● Mean ICP is maintained at less than 15 mmhg Medications: ● Osmotic diuretic such as Mannitol and hypertonic saline 3% ● Pentobarbital for uncontrolled intracranial hypertension Causes: ● Overproduction of CSF, hydrocephalus, interstitial edema, intracranial hemorrhage, hematoma, hypoxia, brain tumor, abscess, brain injury, ischemic stroke, anoxic brain injury, hypoxic encephalopathy, seizures, hyperthermia 12. AKI: Assessment: ● Serum electrolytes, Urine electrolytes, Prerenal Versus Intrarenal. ● Acidosis (pH less than 7.35) one of the trademarks of a severe AKI. Metabolic acidosis occurs as a result of accumulation of waste products in the bloodstream and tissues. ● BUN, Azotemia: Serum creatinine, Creatinine Clearance, Fractional Excretion of Sodium. ● Daily weights (1kg weight gain over 24 hours represents 1000mL of retained fluid) ● Hyperkalemia: 50mLm of 50% dextrose with 10 units of IV regular insulin Treatment: ● Crystalloid vol. Replacement to prevent prerenal failure (0.9 NaCl) ● Fluid restriction during intrarenal failure to prevent circulatory overload ● Diuretics are used to urine output or renal replacement therapy (hemodialysis or hemofiltration) if volume overload exacerbates pulmonary edema or HF ○ Loop diuretics- furosemide ○ Thiazide- chlorothiazide ○ Osmotic- mannitol ○ Carbonic anhydrase inhibitor- acetazolamide ○ potassium sparingspironolactone ● Vaptans (conivaptan) inhibits the effects of ADH (vasopressin) ● Dopamine (2 to 3 mcg/kg/min)- to stimulate blood flow to the kidney ● Acetylcysteine- to assist with expectoration of thick pulmonary secretions, commonly prescribed for pt with mildly elevated serum creatinine levels before radiologic study using contrast dye ● Dietary phosphorus binding meds- to achieve normal calcium levels by reducing the level of phosphorus in the bloodstream ○ 2nd gen dietary phosphorus- calcium carbonate or calcium acetate ○ 3rd gen nonabsorbable dietary phosphorussevelamer hydrochloride and lanthanum carbonate ● Avoid meds excreted by the kidney ● Hemodialysis/CRRT ● Parathyroid hormone helps calcium be absorbed back into the bloodstream to maintain homeostasis ● Calcium replacements such as Vit d and calcium supplements ● If contrast dye is used, aggressive fluid resuscitation with normal saline Nursing interventions, nursing, considerations/prevention: ● Fluid resuscitation with crystalloids, ● hemodynamic, monitoring and fluid balance, ● VS, daily weight, I/O ● Inserting an indwelling urinary cath to record accurate U/O. ● Fluid restriction ● frequent skin care with emollients, discouraging scratching, and administering phosphate-binding meds. ● Monitor ABGs to maintain pH with normal range ● prevent blood loss, minimize blood withdrawal ● because risk for GI bleed, stress ulcer prophylaxis and testing for occult blood with stool, NG tube drainage, and emesis ● educate pt and fam about AKI prognosis, tx, and possible complications 13. CKD: Treatment: ● Maintenance of BP below 130/80 mmHg and blood glucose within normal range ● Manage HTN and fluid balance with antihypertensive meds and diuretics ● Prescribe phosphate binders to control serum phosphate levels (see AKI tx) ● Administer erythropoiesis-stimulating agents to manage anemia ● Peritoneal dialysis (PD) is a less high tech modality used in pt with CKD Assessment: ● Monitor renal function through serum creatinine, GFR, and electrolytes ● Assess complications such as fluid overload , Electrolyte imbalance and anemia Complications of treatments: ● Hypotension with antihypertensive meds ● HyperK from phosphate binders and hypokalemia from diuretics Vascular access complications with AV fistulas or grafts. Care of AV fistulas: ● Avoid wearing constrictive clothing ● Avoid sleeping on or bending accessed limbs for prolonged periods ● Use aseptic technique when cannulating access ● Extremity should be pink and warm to touch ● Has a trill when palpated gently and has bruit when auscultated ● No blood pressure measurements, IV infusion or lab procedures performed on the arm with the fistula ● Complications: Thrombosis, infection, pseudoaneurysm, vascular steal syndrome, venous HTN, carpal tunnel syndrome, Inadequate blood flow 14. GI Bleed: Potentially life threatening Treatment: ● Vagotomy and Pyloroplasty to control bleeding ● Two commonly used endoscopic therapies; endoscopic injection sclerotherapy and endoscopic variceal ligation (EVL) ● If the initial therapies fail, transjugular intrahepatic portosystemic shunt (TIPS) ● Administer vol replacement: 2 large diameter peripheral IV cath should be inserted to facilitate the rapid administration of prescribed fluids. ● Gastric Lavage Medications: ● Histamin-2 (H2) antagonist ( Cimetidine, Ranitidine, Famotidine, Nizatidine) ○ Reduce volume and concentration of gastric secretions ● Proton-pump inhibitors (PPIs) (Omeprazole, Lansoprazole, Rabeprazole, Esomeprazole, Pantoprazole) ○ Inhibits gastric acid secretions by the gastric parietal cells Risk factors: ● Peptic Ulcer Disease ● Stress-related mucosal disease ● Esophagogastric Varices Complications: ● Hypovolemic shock ● Gastric perforation constitute a surgical emergency ( sudden, severe, generalized abdominal pain with significant rebound tenderness and rigidity) ● Perforation should be suspected when fever, leukocytosis, and tachycardia persist despite adequate vol replacement Nursing interventions: ● Airway protection ● Fluid resuscitation to achieve hemodynamic stability such as crystalloids, colloids, and blood and blood products ● Correction of comorbid condition (coagulopathy), therapeutic procedures to stop or control bleeding ● Determine cause of bleeding: Gastric lavage ● Control bleeding: Endoscopic interventions, vasopressin, somatostatin, octreotide, TIPS, surgery (last resort) ● Provide comfort and emotional support ● Maintain surveillance for complications such as hypovolemic shock and gastric perforation ● PT Educ about stress management, diet modifications, alcohol and smoking cessation. 15. Peptic ulcers: pathology, nursing interventions, diagnostic testing, medications,prevention teaching Pathophysiology: - breakdown of gastric mucosal lining - Leading cause of upper GI hemorrhage - erosion - Main cause: Helicobacter pylori and NSAIDS Nursing Interventions: - Maintaining the pH between 3.5 and 4.5 is a goal of prophylactic therapy - Assess for bleeding - Obtain IV access and administer prescribed fluids - Two large-diameter peripheral intravenous cath - Gastric lavage = evacuate blood from the stomach and improve visualization during endoscopy, irrigate with normal saline until the returned solution is clear - Monitor for gastric perforation (surgical emergency) S&S= sudden severe generalized abdominal pain and rebound tenderness and rigidity, fever, leukocytosis and tachycardia despite adequate volume replacement Diagnostic testing: - Fiberoptic endoscopy, tagged red blood scanning, angiography Medications: - Histamine-2 antagonists and proton pump inhibitors - Acid suppressive therapy is associated with increased bacterial colonization of the upper GI tract and increase risk of developing ventilator-associated pneumonia Teaching: - Encourage to stop drinking and refer to alcohol cessation program - Smoking cessation - Stress management 16. GI Obstruction: nursing interventions, post-op care, medications Nursing Interventions: 1. Assessment: ● Conduct a thorough assessment of the patient's medical history, including any previous abdominal surgeries, gastrointestinal disorders, or risk factors for obstruction (e.g., adhesions, tumors). ● Monitor vital signs and assess for signs and symptoms of GI obstruction, including abdominal pain, distension, nausea, vomiting, constipation, and inability to pass flatus or stool. 2. Fluid and Electrolyte Management: ● Assess for signs of dehydration and electrolyte imbalances, such as hypovolemia, tachycardia, hypotension, and electrolyte abnormalities on laboratory tests. ● Administer intravenous fluids and electrolytes as prescribed to restore fluid balance and maintain hydration. 3. NG Tube Management: ● Insert a nasogastric (NG) tube to decompress the stomach and relieve distension in cases of partial or complete obstruction. ● Monitor NG tube output for volume, color, and consistency, documenting findings accurately. ● Assess for complications of NG tube placement, such as mucosal damage, aspiration, or tube dislodgement. 4. Pain Management: ● Administer analgesics as prescribed to relieve abdominal pain and discomfort. ● Use non-pharmacological pain relief measures such as positioning, relaxation techniques, and heat therapy to complement pharmacological interventions. Post-Operative Care: 1. Monitoring: ● Monitor for signs of post-operative complications, such as infection, hemorrhage, bowel perforation, or anastomotic leakage. ● Assess surgical incision sites for signs of infection, including redness, swelling, warmth, and purulent drainage. 2. Bowel Function: ● Assess bowel sounds regularly to monitor for return of peristalsis and resolution of obstruction. ● Monitor bowel movements and assess stool consistency and frequency to evaluate gastrointestinal function post-operatively. 3. Nutritional Support: ● Initiate enteral or parenteral nutrition as prescribed to meet the patient's nutritional needs and support healing. ● Monitor for signs of malnutrition and adjust nutritional support accordingly to prevent complications such as protein-energy malnutrition and delayed wound healing. Medications: 1. Antiemetics: ● Administer antiemetic medications such as ondansetron or metoclopramide to relieve nausea and vomiting associated with GI obstruction. ● Monitor for side effects such as sedation, dizziness, and extrapyramidal symptoms. 2. Analgesics: ● Administer analgesic medications such as acetaminophen or opioids to relieve pain and discomfort. ● Use caution when administering opioids in patients with GI obstruction, as they can cause respiratory depression and exacerbate constipation. 3. Antibiotics: ● Administer prophylactic or therapeutic antibiotics as prescribed to prevent or treat postoperative infections, especially in cases of bowel resection or perforation. ● Monitor for signs of antibiotic-associated adverse effects, such as allergic reactions, gastrointestinal upset, or Clostridium difficile infection. Discharge Planning: 1. Patient Education: ● Provide discharge instructions to the patient and caregivers regarding post-operative care, including wound care, activity restrictions, medication management, and signs of complications. ● Educate patients on dietary modifications, including recommendations for a low-fiber or bland diet during the recovery period. 2. Follow-Up Care: ● Schedule follow-up appointments with the healthcare provider to monitor recovery progress and evaluate for resolution of symptoms. ● Provide contact information for emergency services and instructions on when to seek medical attention for worsening symptoms or signs of complications. 17. Liver failure: complications, treatment, nursing interventions, risk factors,medications Complications - Bleeding - Must be on bleeding precautions - Hypoglycemia, metabolic acidosis, hypokalemia and hyponatremia should be monitored - High risk for infection - ICP - manage with mannitol but be cautious with pt with renal failure to avoid hyperosmolality - Hemodynamic instability is a common complication Treatment and Medication - Antibiotics such as neomycin, metronidazole and rifaximin and lactulose - LACTULOSE - gold standard - Antibiotics reduce bacterial flora of the colon = aids in decreasing ammonia formation by decreasing bacterial action on the protein in feces - Lactulose - synthetic ketoanalogue of lactose split into lactic and acetic acid in the intestine. Given orally through an NG tube or retention enema. Nursing Interventions 1. Protect the patient from injury - Use of benzos and sedatives is discouraged because pertinent - neurologic changes may be masked and hepatic encephalopathy may be exacerbated Patient are usually extremely agitated and combative = physical restraint may be necessary to prevent injury 2. Maintenance Surveillance for complications - Respiratory depression and arrest can occur quickly - Continuous pulse oximetry monitoring and abg - Thorough neurologic assessment every hour Risk Factors - Infections, medications, toxins, hypoperfusion, metabolic disorders and surgery - Viral hepatitis and medication-induced liver damage - Budd-Chiari syndrome (blocked venous outflow from small hepatic veins to inferior vena cava from thrombosis - Reye syndrome, Wilson disease (defective copper metabolism that damages liver and brain), galactosemia (rare disease in infants in which they cannot metabolize galactose, resulting in hepatocellular damage), and fructose intolerance 18. Pancreatitis: risk factors, diagnostic tests, nursing interventions, treatment Risk Factors - Alcohol - Biliary disease - Hypertriglyceridemia - Toxins - Thiazides, immunosuppressive agents, antiinflammatory drugs - Hypercalcemia - Tumor - Infections - Trauma - Hypoperfusion - Vasculitis - Pregnancy - Hypothermia - Sphincter of Oddi dysfunction - Autoimmune diseases - Ampullary stenosis - Idiopathic cause Diagnostic tests - Abdominal ultrasound can - CECT - gold standard - MRI - for pt at risk for contrast related complications Nursing Interventions 1. Provide Comfort and Emotional Support - Pain management is a PRIORITY - Morphine, fentanyl and hydromorphone - Relaxation techniques and knee-chest position assist in pain control 2. Maintenance and surveillance for complications - Organ failure is a major indicator of the severity of the disease - Intraabdominal pressure monitoring is initiated if intra abdominal hypertension is suspected - Monitor for pancreatic infection - Persistent Abdominal pain - Abdominal tenderness - Prolonged fever - Abdominal distention - Prolonged fever - Palpable abdominal mass - Nausea and vomiting - Increase wbc - Persistent elevation of serum amylase - Hyperbilirubinemia - Elevated Alkaline Phosphate level - Positive culture and gram stain Treatment - Ensuring adequate pain management, fluid and electrolyte replacement, providing nutrition support and correct metabolic complications 1. Fluid Management - - - - - - Intravenous crystalloids administered immediately to prevent hypovolemic shock Monitor for hypocalcemia, hypokalemia, hypomagnesemia If hyperglycemia develops = exogenous insulin administered Ringer’s lactate may be superior to 0.9% sodium chloride solution due to antiinflammatory effects of the lactate Fluids should be administered 5 to 10 mL/kg/h Aggressive fluid resuscitation should be avoided 2. Nutrition support - Start oral feedings within 24 hours to protect the gut-mucosal barrier and reduce incidence of bacterial translocation - Pt who are unable to take oral feedings should be started on enteral feedings via nasogastric or nasoenteric (duodenal or jejunal) - Enteral feeding is preferred over parenteral nutrition - Parenteral nutrition is only indicated if the patient is unable to tolerate enteral nutrition 19. Thrombocytopenia: risk factors, pathology, nursing interventions, treatment - - Platelet count less than 150,000 or a decrease of greater than 50% from the last measurement Mild - 70,000 to 150,000 Moderate - 20,000 to 70,000 Severe - less than 20,000 50,000 risk for bleeding Risk Factors - Viral infection - Pregnancy - Administration of heparin, thiazide, diuretics, chemo agents - Malignancies - Splenomegaly - Blood transfusion - alcoholism - Medical Management - IV immunoglobulin to suppress platelet destroying antibody - High dose methylprednisolone through IV - Platelet transfusion - Surgical removal of spleen Nursing Interventions - Bleeding precaution - Padding side rails - Firm bristled toothbrush - Blow nose slowly - Electric razor - Avoid venipuncture and IM 20. HIT: pathology, risk factors, nursing interventions, treatment - Pathology - Decrease platelet - Increase platelet destruction - Splenic sequestration - Massive consumption of platelets - Hemodilution - Lymphocytes produce antibodies to destroy platelets Manifestations - Petechial hemorrhages (platelet) - Large hematoma (coagulation disorder) - Unusual bleeding is a hallmark Bleeding gums, spontaneous epistaxis, blood in urine or stool, heavy mens, retinal hemorrhage or intracerebral bleeding - Severe thrombocytopenia during heparin treatment Less than 50000 Occurs 5 to 10 days Pathology - Formation of heparin-antibody complexes (platelet factors) - Platelet factor 4 attracts heparin molecule, forming immunogenic complexes that adhere to platelet stimulates the release of thrombin and the subsequent formation of platelet clumps - - - Vessel occlusion can result in the need for limb amputation, stroke, acute MI and death Formation of fibrin and platelet rich thrombi is the primary characteristic White clot syndrome Risk Factors - Higher in women - Surgical patients - Patients with major trauma - Cardiac and orthopedic surgery Treatment - Platelet monitoring every 2 or 3 days from day 4 to day 14 - Direct thrombin inhibitors - bind directly to thrombin molecule, inhibiting its actions - Argatroban only medication approved Nursing Interventions - All heparin removed from the patient’s hemodynamic pressure monitoring system - Avoid use of heparin-coated catheters and discontinue heparin flushes to maintain the patency of iv - Monitor for dvt and prevent dvt 21. Sickle cell anemia: nursing interventions, pathology, nursing assessment, symptoms - Hereditary disease - - Abnormal sickle or crescent shape rbc Sickle cell has short lifespan and unable to carry adequate oxygen and become trapped in the vasculature and cause severe pain and increased risk of infection Autosomal recessive genetic African, caribbean, central american, south american, saudi arabian, indian, mediterranean descent Pathology - Chronic inflammatory condition that is characterized by hemolysis and vasoocclusion - Hbs production - Occur during times of physiologic stress such as physical overexertion, muscle tissue ischemia, dehydration, infection, or extreme temperatures Nursing Assessment - Low-grade fever, bone or joint pain, pinpoint pupils inability to follow commands, photophobia, tachycardia, tachypnea, decreased respiratory excursion, hepatomegaly, nonpalpable spleen, pretibial ulcers - Sickle cell constitutes 5% to 10% of the blood smear - Elevated reticulocyte count (> 10%) is characteristically accompanied by the presence of howell-jolly bodies - Elevated wbc - Elevated Indirect bilirubin Hemolysis Haptoglobin level will be low or absent Treatment 1. Prevent infection a. Prophylactic administration of oral antibiotics b. Vaccinations against pneumococcal infection, meningitis, hepatitis, and influenza 2. Pain Management a. Common pain - vaso occlusive pain b. Treated with anti inflammatory and nonopioid agents c. Paracetamol and nsaids for mild to moderate pain d. Oral or parenteral opiates for severe e. Massage, acupuncture, transcutaneous electrical nerve stimulation f. Television, video games, repeating inspirational phrases and mental calculations g. Cognitive behavioral therapy 3. Transfusion therapy a. Transfusion therapy is primarily used for treatment of patients who are experiencing complications secondary to SCD b. Used with caution due to risk for iron overload, exposure to hepatitis, HIV c. Indication is recurrent painful vaso occlusive crises, acute chest syndrome, stroke, priapism and leg ulcers 4. Administration of Hydroxyurea a. Increase the level of fetal hemoglobin in the rbcs and reduces concentrationd of sickle hgb and sickling itself b. Starts at 15 mg/kg po once a day c. Increase 5 mg/kg every 12 weeks until 35 mg/kg is reached Nursing Interventions - - - - Administration of iv fluids, blood products and inotropic agents Monitor vs, hemodynamic parameters, intake and output Assess neurologic status, kidney function cardiopulmonary status, skin integrity Mental status, BUN, creatinine. Urine output, cardic rhythym, abg and pulse oximetry, ecchymoses, hematomas Monitor for complication such as septicemia, acute myocardial infarction, priapism, ischemic stroke and shock Smoking cessation 22. Shock: types, treatment of types, signs and symptoms 1. Hypovolemic shock a. Inadequate fluid volume in the intravascular space b. Decreased tissue perfusion c. Decreased sv and co Assessment - Class I/ Mild shock - fluid volume loss up to 15% to 20% or 750 mL - Free of symptoms, possibly anxiety - Class II/ Moderate shock 15% to 30% or 750 to 1500 mL - Anxiety increases, hr more than 100 bpm, pulse pressure narrows as the diastolic blood pressure increases, postural hypotension, rr increases, respiratory alkalosis, urine output decline to 20-30 ml/h urine sodium level decrease, urinary osmolality and specific gravity increase as the kidney starts to conserve sodium and water, pt skin pale and cool with delayed cap refill, jugular veins appear flat - Class III - 30 to 40% or 1500 to 2000 mL - Bp decrease, hr >120 bpm, dysrhythmias may develop as myocardial ischemia, serum lactate increase, metabolic acidosis, oliguria, increase bun and creatinine, skin ashen cold and clammy, marked delay cap refill, confusion due to cerebral perfusion decrease - Class IV/Severe - greater than 40% or greater than 2000 m - Severe lactic acidosis, peripheral pulses and cap refill absent, skin cyanotic, mottled and extremely diaphoretic, organ failure, ot confused agitated and unresponsive Management - Administer crystalloid solution, colloid solution, blood products, or a combination of fluids - Aggressive fluid resuscitation - Administer vasopressor Nursing Management - Monitor I&O - Daily weight - Evaluation of intravascular volume, tissue perfusion, response therapy - Minimize fluid loss - Limit blood sampling, observe lines for accidental disconnection and applying direct pressure to bleeding sites - Monitor organ failure 2. Cardiogenic Shock Description and Etiology: a. Cardiogenic shock occurs due to the heart's failure to pump blood effectively, resulting in decreased tissue perfusion and circulatory failure. b. Dysfunction of the right or left ventricle, or both, contributes to cardiogenic shock. c. It affects approximately 5% to 8% of patients with ST segment myocardial infarction (MI) and is a leading cause of death in MI patients. d. Mortality rates have decreased with early revascularization therapy, but remain high at approximately 40% to 65%. e. Causes include acute MI, cardiomyopathy, severe valvular disease, acute ruptures, cardiac tamponade, and massive pulmonary embolism. Pathophysiology: f. Cardiogenic shock results from impaired ventricular pumping ability, leading to decreased stroke volume (SV) and cardiac output (CO), and ineffective tissue perfusion. g. Compensatory mechanisms, including vasoconstriction, worsen myocardial ischemia. h. Left ventricular failure leads to pulmonary congestion and edema, impairing gas exchange and oxygenation. i. Inflammatory cytokines may contribute to systemic vasodilation, impacting CO. j. Cardiopulmonary collapse or multiple-organ failure can lead to death. Assessment and Diagnosis: k. Clinical manifestations reflect decreased CO, including low blood pressure, altered mental status, cool and pale skin, decreased urine output, chest pain, tachycardia, weak pulse, and respiratory distress. l. Lung auscultation may reveal crackles and rhonchi, indicating pulmonary edema. m. Hemodynamic assessment shows decreased CO, elevated pulmonary artery occlusion pressure (PAOP), and increased systemic vascular resistance (SVR). n. Echocardiography confirms diagnosis and provides noninvasive estimates of PAOP and ejection fraction. Medical Management: o. Treatment aims to address underlying causes, enhance pump effectiveness, and improve tissue perfusion. p. Inotropic agents like dobutamine increase contractility. q. Vasopressors like norepinephrine may be used to maintain blood pressure. r. Diuretics reduce preload, while vasodilators reduce preload and afterload. s. Mechanical circulatory assist devices like intra aortic balloon pump (IABP) or ventricular assist devices (VAD) can be used if tissue perfusion cannot be immediately restored. t. Emergent revascularization and fibrinolytic agents may be used in acute MI. Nursing Management: u. Prevention includes identifying at-risk patients, facilitating early reperfusion therapy, and frequent cardiopulmonary assessment. v. Nursing interventions focus on limiting myocardial oxygen demand, enhancing oxygen supply, maintaining tissue perfusion, providing comfort and emotional support, and preventing complications. w. Close monitoring and management of hemodynamic variables, respiratory function, and dysrhythmias are essential. x. Patients on mechanical devices need frequent observation for complications like infection, bleeding, and thrombosis. - 3. Neurogenic Shock -Lack of sympathetic tone leads to decreased tissue perfusion -The most common cause is spinal cord injury (SCI) -Spinal cord injury results in a loss of sympathetic tone -> massive peripheral vasodilation, inhibition of baroreceptor response, & impaired thermoregulation. Assessment / Signs & Symptoms: - Hypotension - massive peripheral vasodilation -Bradycardia - inhibition of baroreceptor response & unopposed parasympathetic control of heart -Warm, Dry skin- blood pooling in extremities and loss of vasomotor control in surface vessels of the skin that control heat loss -Hypothermia - uncontrolled peripheral heat loss - Increased Anxiety - Increased RR - ABG’s - respiratory alkalosis - Decreased PAC02 - Flat jugular veins - Urine output below 30 ml/hr Medical Management: - Vasopressors *If needed, atropine, IV beta-blocker, or pacemaker to treat Bradycardia Hypothermia temperature regulation Preventative care: Identify at-risk patients and assess neurologic status regularly. Immobilization of spinal cord injuries and slight elevation of the head of the patient's bed after spinal anesthesia. Monitor closely for hypovolemia, bradycardia, and hypothermia. Fluid resuscitation as needed to ensure tissue perfusion. Use vasopressors to maintain blood pressure and organ perfusion. Manage hypothermia with warming measures and environmental temperature regulation. 4. Anaphylactic shock Description and Etiology: a. Anaphylactic shock is a severe and immediate hypersensitivity reaction that leads to systemic vasodilation, increased capillary permeability, and bronchoconstriction, resulting in decreased tissue perfusion. b. Triggers of anaphylaxis include immunologic antibody-antigen reactions or non-immunologic mast cell and basophil activation. These triggers c. d. e. f. encompass a wide range of substances, including foods, medications, environmental allergens, and physical stimuli. Immunologic reactions can be IgE-mediated or non-IgE-mediated. IgE-mediated reactions involve the formation of antigen-specific IgE antibodies, leading to mast cell sensitization and subsequent release of histamine and other mediators upon re-exposure to the antigen. Non-IgE-mediated reactions involve direct activation of mast cells and basophils or other immune pathways, leading to mediator release. Latex is a significant antigen of concern in healthcare settings due to its presence in many medical products. Mast cell activation and mediator release cause a cascade of physiological responses, including vasodilation, increased vascular permeability, smooth muscle contraction, and inflammation. Pathophysiology: g. Immunologic and non-immunologic activation of mast cells and basophils result in the release of various biochemical mediators, including histamine, tryptase, leukotrienes, prostaglandins, and cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). h. Histamine and other mediators cause widespread effects throughout the body, including vasodilation, increased capillary permeability, bronchoconstriction, and smooth muscle contraction in the gastrointestinal and genitourinary systems. i. Vasodilation leads to relative hypovolemia and decreased venous return, reducing cardiac preload and output. Increased capillary permeability results in fluid leakage into tissues, exacerbating hypovolemia and compromising tissue perfusion. j. Coronary vasoconstriction may occur, leading to myocardial depression and impaired cardiac function. k. The combination of vasodilation, hypovolemia, and impaired cardiac function culminates in systemic hypoperfusion, potentially leading to cardiovascular collapse and organ failure. Assessment and Diagnosis: l. m. n. o. p. Anaphylactic shock presents with a spectrum of clinical manifestations, including cutaneous, respiratory, gastrointestinal, and cardiovascular symptoms. Cutaneous symptoms such as pruritus, urticaria, and angioedema are common early signs, often followed by respiratory distress, including wheezing, stridor, and dyspnea. Gastrointestinal symptoms such as abdominal pain, vomiting, and diarrhea may occur due to smooth muscle contraction. Cardiovascular manifestations include hypotension, tachycardia, and eventually, circulatory collapse. Assessment of hemodynamic parameters reveals decreased cardiac output and cardiac index, as well as changes in preload, afterload, and systemic vascular resistance. Medical Management: q. Immediate treatment aims to remove the offending antigen, stabilize the patient's airway, ventilation, and circulation, and reverse the effects of biochemical mediators. r. Epinephrine is the cornerstone of therapy, acting to counteract vasodilation, bronchoconstriction, and mediator release. Intramuscular injection is preferred for mild cases, while intravenous administration is indicated for severe cases with hypotension. s. Oxygen therapy, intubation, and mechanical ventilation may be necessary to maintain adequate oxygenation and ventilation. t. Rapid volume replacement with crystalloid or colloid solutions helps restore intravascular volume and improve tissue perfusion. u. Vasopressors may be required to support blood pressure in refractory cases. v. Adjunctive therapies include antihistamines, corticosteroids, and inhaled beta-adrenergic agents to address specific symptoms and prevent recurrence. Nursing Management: w. Prevention involves identifying at-risk patients, obtaining detailed allergy histories, and avoiding known triggers. x. Nursing interventions focus on rapid recognition and initiation of treatment, including administering epinephrine, ensuring airway patency, and providing fluid resuscitation. y. Ongoing assessment of the patient's response to treatment, vital signs, and hemodynamic status is critical. z. Patient education on allergen avoidance, recognition of symptoms, and self-administration of epinephrine is essential for long-term management and prevention of future episodes. 4.Septic Shock Description and Etiology: ● Sepsis is a life-threatening syndrome resulting from infection and a dysregulated systemic response. ● Septic shock involves severe complications and higher mortality risk than sepsis. ● Mechanisms include blood flow maldistribution, hypovolemia, and myocardial dysfunction. ● Common microbial sources include bacteria, fungi, and viruses from various bodily systems. ● Pathophysiology: ● Initiated by microbial invasion triggering inflammatory/immune responses. ● Systemic activation leads to clotting abnormalities, microvascular thrombosis, and endothelial damage. ● Cardiovascular alterations include impaired ventricular contractility and peripheral vasodilation. ● Metabolic changes involve increased lactate production, insulin resistance, and mitochondrial dysfunction. ● Cellular hypoxia, damage, and apoptosis occur, contributing to multiple-organ dysfunction syndrome (MODS). ● Assessment and Diagnosis: ● Early recognition vital; Sequential (Sepsis-related) Organ Failure Assessment (SOFA) score assists in identifying dysfunction. ● Clinical signs include hypotension despite fluid resuscitation, perfusion abnormalities, and pulmonary dysfunction (ARDS). ● Patients may present with dynamic clinical manifestations reflecting the progression of the condition. ● Medical Management: ● Multifaceted approach targeting infection control, reversal of pathophysiologic responses, and metabolic support. ● Early treatment improves outcomes; adherence to established guidelines crucial. ● Hour-1 Bundle emphasizes interventions within the first hour. ● Immediate resuscitation involves fluid administration, vasopressors, and possibly inotropic agents. ● Antibiotic therapy should commence promptly, with source identification within 6 hours. ● Other interventions include mechanical ventilation, stress ulcer prophylaxis, and DVT prophylaxis. ● Nursing Management: ● Focus on infection prevention, early recognition, and supportive care. ● Preventive measures include handwashing, aseptic technique, and ongoing surveillance. ● Continuous observation for subtle changes indicating sepsis progression is crucial. ● Nursing interventions encompass administering prescribed treatments, providing comfort and emotional support, and preventing complications. ● Emphasis on evidence-based practice to prevent further compromise and improve patient outcomes. 23. Carbon monoxide poisoning: signs and symptoms, treatment, nursing interventions Signs and Symptoms: 1. Initial Symptoms: ● Headache ● Dizziness ● Weakness ● Nausea ● Vomiting ● Confusion ● Shortness of breath ● Chest pain ● Visual disturbances ● Altered mental status 2. Progressive Symptoms: ● Cyanosis (cherry-red skin color in severe cases) ● Seizures ● Loss of consciousness ● Coma ● Respiratory failure ● Cardiac arrest Treatment: 1. Remove from Exposure: ● Move the patient to fresh air immediately to prevent further exposure to carbon monoxide. 2. Administer Oxygen Therapy: ● Administer high-flow oxygen therapy via a non-rebreather mask to maximize oxygen delivery and eliminate carbon monoxide from the bloodstream. ● Use hyperbaric oxygen therapy (HBO) in severe cases to rapidly decrease carboxyhemoglobin levels and prevent long-term neurological sequelae. 3. Monitor Vital Signs: ● Monitor vital signs closely, including oxygen saturation, respiratory rate, heart rate, blood pressure, and level of consciousness. ● Obtain baseline arterial blood gas (ABG) measurements to assess for hypoxemia and acid-base disturbances. 4. Assess for Complications: ● Monitor for complications such as myocardial ischemia, arrhythmias, neurological deficits, and acute respiratory distress syndrome (ARDS). ● Perform continuous cardiac monitoring and neurological assessments to detect changes in status promptly. Nursing Interventions: 1. Airway Management: ● Assess and maintain a patent airway, ensuring adequate oxygenation and ventilation. ● Prepare for advanced airway management techniques such as endotracheal intubation in cases of respiratory failure or decreased level of consciousness. 2. Fluid Resuscitation: ● Administer intravenous fluids cautiously to maintain adequate tissue perfusion and prevent hypotension. ● Monitor fluid balance closely, adjusting fluid rates based on ongoing assessment of hemodynamic status and urine output. 3. Neurological Assessment: ● Assess level of consciousness using standardized scales such as the Glasgow Coma Scale (GCS). ● Monitor for neurological deficits such as confusion, agitation, seizures, and focal motor deficits. 4. Temperature Regulation: ● Monitor core body temperature closely, as carbon monoxide poisoning can lead to hypothermia due to impaired thermoregulation. ● Provide warming measures such as blankets or forced air warming devices as needed to maintain normothermia. 5. Psychosocial Support: ● Provide emotional support to patients and families affected by carbon monoxide poisoning, addressing concerns and providing information about the condition and treatment. ● Refer patients to appropriate support services such as social work or counseling for ongoing support and coping strategies. Education and Prevention: 1. Education: ● Educate patients and caregivers about the dangers of carbon monoxide poisoning and methods to prevent exposure, such as proper maintenance of heating systems, installation of carbon monoxide detectors, and avoidance of using charcoal grills or portable generators indoors. 2. Follow-Up Care: ● Emphasize the importance of follow-up care with healthcare providers to monitor for delayed complications and assess for resolution of symptoms. ● Provide written instructions and resources for home safety measures and emergency preparedness. 3. Community Outreach: ● Participate in community outreach programs to raise awareness about carbon monoxide poisoning and promote preventive measures in high-risk populations, such as older adults, children, and individuals with chronic medical conditions. 24. Burns: nursing interventions, nursing assessment, complications, interventions to prevent complications Assessment Tools: ● Use tools such as the Rule of Nines or Lund and Browder chart for accurate estimation of burn extent and depth. ● Classify burns based on degree: ● First-Degree Burns: Superficial burns involving only the epidermis, characterized by erythema, pain, and mild swelling. ● Second-Degree Burns: Partial-thickness burns involving the epidermis and varying depths of the dermis, characterized by blistering, erythema, pain, and edema. ● Third-Degree Burns: Full-thickness burns involving the entire dermis and possibly deeper tissues, characterized by white, brown, or black eschar, insensitivity to pain due to nerve damage, and potentially charred tissues. ● Document mechanism of injury, time elapsed since burn occurrence, and any associated injuries, such as inhalation injury from smoke exposure. Nursing Interventions: ● Airway Management: ● Assess and maintain a patent airway, ensuring adequate oxygenation and ventilation. ● Administer supplemental oxygen as needed to maintain oxygen saturation levels. ● Prepare for advanced airway management techniques such as endotracheal intubation or surgical airway placement in cases of severe airway compromise. ● Fluid Resuscitation: ● Calculate fluid resuscitation requirements using validated formulas such as the Parkland formula or modified Brooke formula. ● Initiate fluid resuscitation promptly to replace fluid losses and maintain tissue perfusion. ● Monitor fluid balance closely, adjusting fluid rates based on ongoing assessment of patient response and hemodynamic status. ● Wound Care: ● Cleanse burns gently with mild soap and water to remove debris and minimize infection risk. ● Apply appropriate dressings based on burn depth and location, considering factors such as moisture balance, adherence, and antimicrobial properties. ● Monitor wound healing progress and assess for signs of infection, such as erythema, warmth, or purulent drainage. ● Pain Management: ● Administer analgesics as prescribed, using a multimodal approach to address both nociceptive and neuropathic pain. ● Incorporate non-pharmacological pain relief strategies such as positioning, distraction, relaxation techniques, and guided imagery. ● Assess for potential side effects of pain medications, including respiratory depression, sedation, and gastrointestinal disturbances. ● Prevention of Complications: ● Implement measures to prevent infection, including strict hand hygiene, aseptic technique during wound care, and administration of prophylactic antibiotics as indicated. ● Monitor for and manage complications such as compartment syndrome, inhalation injury, and hypovolemia promptly to prevent further tissue damage and organ dysfunction. ● Provide nutritional support to optimize wound healing and prevent malnutrition, collaborating with dietitians to develop individualized feeding plans based on nutritional needs and preferences. Complications: ● Infection: ● Monitor for signs of wound infection, such as increased pain, erythema, swelling, or purulent drainage. ● Collect wound cultures as needed to identify pathogens and guide antibiotic therapy. ● Educate patients and caregivers on proper wound care techniques and signs of infection to report promptly. ● Hypovolemic Shock: ● Monitor fluid balance closely, assessing for signs of hypovolemia such as tachycardia, hypotension, and decreased urine output. ● Administer intravenous fluids judiciously to maintain adequate perfusion without exacerbating edema or fluid overload. ● Compartment Syndrome: ● Monitor for signs and symptoms of compartment syndrome, including severe pain disproportionate to injury, tense swelling, and paresthesia. ● Measure compartment pressures as indicated, considering fasciotomy for decompression in cases of suspected compartment syndrome to prevent irreversible tissue ischemia and necrosis. Additional Interventions: ● Early Mobilization: ● Initiate early mobilization and range of motion exercises to prevent contractures and maintain joint function. ● Collaborate with physical and occupational therapists to develop individualized rehabilitation plans and maximize functional outcomes. ● Psychosocial Support: ● Provide emotional support to patients and families coping with the physical and psychological effects of burns. ● Refer patients to support groups, counseling services, or peer mentors to facilitate coping and adjustment to life after burn injury. ● Scar Management: ● Initiate scar management interventions early in the healing process to minimize scar formation and improve cosmetic outcomes. ● Use techniques such as pressure garments, silicone gel sheets, and massage therapy to soften and flatten scars and promote tissue remodeling. ● Patient Education: ● Educate patients and caregivers on signs of wound infection, proper wound care techniques, and strategies to prevent complications such as falls, pressure injuries, and venous thromboembolism. ● Provide resources and written instructions for home care management and follow-up appointments to promote continuity of care and facilitate optimal outcomes. Medications: ● Topical Antimicrobial Agents: ● Silver Sulfadiazine and Mafenide Acetate: Prevent and treat infection in burn wounds by inhibiting microbial growth. ● Systemic Antibiotics: ● Administered for established infection or high infection risk, based on culture and sensitivity results. ● Pain Management: ● Opioids, NSAIDs, and adjuvant medications used to alleviate pain associated with burns. Inhalation Injury: Assessment: ● Evaluate for signs and symptoms such as singed nasal hair, facial burns, hoarseness, soot in the airway, or carbonaceous sputum. ● Use fiberoptic bronchoscopy or bronchial lavage for definitive diagnosis. Management: ● Maintain a high index of suspicion for airway compromise and early intubation if necessary. ● Administer supplemental oxygen and bronchodilators to optimize respiratory function. ● Use corticosteroids cautiously to reduce airway inflammation. Complications: ● Respiratory failure, ARDS, pneumonia, or airway obstruction may develop, requiring vigilant monitoring and intervention. 25. Diabetes: types, pathology behind each type, complications - Diagnosed by fasting plasma glucose or glycated hemoglobin A1c greater than 6.5% FPG: - Level 70 to 100 mg/dL = normal - 100 and 124 mg/dL = impaired fasting glucose - Greater than 126 mg/dL = diagnostic of diabetes Type 1 Diabetes - Progressive destruction of the beta cells if the islet of Langerhans in the pancreas - Occurs rapidly in some patient (mainly children) - Ketoacidosis as the first manifestations - Prone to development of Graves disease, hashimoto thyroiditis, addison disease, autoimmune hepatitis, myasthenia gravis and pernicious anemia - IV or subcutaneous insulin - DKA complication Type 2 Diabetes - Decreased insulin secretion and insulin resistance - Occurs gradually - Usually obese - Managed by oral medications - Insulin resistance - organ and tissue deny entry to insulin and glucose - Managed by lifestyle management (weight reduction, increased physical exercise and a change in diet) 26. DKA: diagnostic tests, risk factors, nursing interventions, treatment, complications, assessment, signs and symptoms, medications Diagnostic test - Blood glucose greater than 250 mg/dL - pH less than 7.3 - Serum bicarbonate less than 18 mEq/L - Moderate or severe ketonemia or ketonuria Risk Factor - Infection - Sick days Nursing interventions 1. Administer fluids, insulin and electrolytes - Use of volumetric pump - Kept on NPO status until hyperglycemia is under control - Fall in glucose 50 to 70 mg/DL per hour - When blood glucose falls to or below 200 = D5W with 0.45% NaCl solution is infuse to prevent hypoglycemia, insulin per hour will be decrease - Goal to maintain blood glucose between 140 to 200 until ketoacidosis subsides 2. Monitoring response to therapy - Monitor accurate I&O - Hourly urine output - VS esp HR, hemodynamic values and Bp - Monitor pulse - Monitor respirations - Blood glucose monitored each hour 3. Surveillance for complications - Fluid volume overload. Hypoglycemia, hypokalemia, hyperkalemia, hyponatremia, cerebral edema and infection a. Fluid volume overload i. Neck vein engorgement, dyspnea without exertion, pulmonary crackles ii. Reduce rate, elevate head of bed, provide oxygen iii. Hourly urine measurements b. Hypoglycemia i. Less than 70 mg/dL ii. Unexpected behavior changes or decreased level of consciousness, diaphoresis and tremors are warning signs c. Hypokalemia and hyperkalemia i. Hypokalemia can occur within the first hours of rehydration and insulin treatment ii. Continuous cardiac monitoring for dysrhythmias iii. Hyperkalemia occurs with acidosis iv. Severe hyperkalemia- large peaked T wave, flattened P wave and widened QRS v. Ventricular fibrillation can follow d. Hyponatremia i. Elimination of sodium results from the osmotic diuresis and is compounded by vomiting and diarrhea that can occur during DKA ii. Abdominal cramping, postural hypotension and unexpected behavioral changes iii. NaCl is infused as the initial IV solution e. Level of consciousness i. Alterations in LOC, pupil reaction and motor function may ii. iii. be the result of fluctuating glucose levels and cerebral fluid shifts Confusion and sudden complaints of headache are ominous signs of cerebral edema Neurologic assessment performed every hour during acute phase 4. Skin care - Dehydration, hypovolemia and hypophosphatemia interfere with oxygen delivery at the cell site and contribute to inadequate perfusion and tissue breakdown - Patient must be reposition every 1-2 hours 5. Oral care - Sponge sticks or moist gauze pads can be used for unconscious patients - Swabbing mouth moistens the tissues and displaces the bacteria that collect when saliva. Which has bacteriostatic action, is curtailed by dehydration 6. Infection Prevention - Strict sterile technique - Venipuncture assess every 4 hrs for inflammation, phlebitis or infiltration - Urinary catheter care is provided every 8 hours 7. Teaching - Take insulin even when sick Treatment 1. Reverse dehydration a. Aggressive Iv fluid replacement b. Assessment of hydration is the important first step c. Iv Isotonic normal saline d. Severe dehydration= 1L of NS e. Serum osmolality high and hypernatremia = hypotonic Nacl (0.45) follow with initial slime replacement f. Replacement infusion typically includes 20 to 30 mEq of potassium per litter g. After serum glucose decreased to 200 = iv solution changed to a 50/50 mix of hypotonic saline and 5 % dextrose. h. Dextrose is added to replenish depleted cellular glucose i. Dextrose infusion also prevents unexpected hypoglycemia 2. Insulin administration a. Moderate to severe = initial iV bolus of regular insulin at 0.1 unit for each kg of body weight with continuous infusion of regular insulin at 0.1 unit/kg/h is infused simultaneously with IV fluid replacement b. Blood glucose check every hour then decrease to 2-4 hrs 3. Reversing ketoacidosis a. Replacement of fluid volume and insulin interrupts the ketotic cycle and reverses the metabolic acidosis. In the presence of insulin, glucose enters the cells, and the body ceases to convert fats into glucose b. Adequate hydration and insulin replacement usually correct acidosis c. Indwelling arterial line provides access for hourly sampling of abg to evaluate pH, bicarbonate and other lab values d. Hyperglycemia usually resolves before ketoacidemia e. May require 6-9 L of IV fluids replacement f. Volume resuscitation occurs over 24 to 36 hours with most iv crystalloid administered in the first 8 hrs 4. Replenishing electrolytes a. Low serum potassium levels occurs as insulin promotes return of potassium into the cell and b. c. d. e. metabolic acidosis is reversed K level must be 3.3 mEq or greater before administering insulin Potassium levels must be monitored Potassium chloride is administered as soon as serum potassium levels are low Phosphate replacement if less than 1 mg/d Assessment - Greater than 250 mg/DL - Ketoacidosis - Low pH less than 7.3 - Metabolic acidosis - Dehydration - Polyuria, glycosuria - Acetone breath - Kussmaul's respirations - Malaise, headache, polyuria, polydipsia, polyphagia, nausea, vomiting, extreme fatigue, dehydration and weight loss - May be stuporous or unresponsive - flushed dry skin, dry buccal membrane, skin turgor more than 3 seconds - Tachycardia and hypotension 27. Hyperthyroid: complication (signs and symptoms of complications), treatments Complications - Thyroid Storm - Aka Thyrotoxicosis Primary cause is Graves disease Caused by stopping antithyroid medications and major stressors such as infection, surgery,trauma, pregnancy or critical illness Signs and Symptoms - Hyperactivity of cardiac tissue, nervous tissue, and smooth muscle tissue and tremendous heat production with elevated temperature - Metabolic acidosis is a potential problem - Muscular breakdown - Malnutrition and weight loss - Fever, afib, sv, acute hf, agitation, restlessness, delirium, nausea, vomiting, diarrhea, unexplained jaundice, stupor coma - A score of greater than 45 is indicative of thyroid storm - Tsh is low and T3 t4 high Medical Management 1. Prevent cardiovascular collapse a. Beta blockers are mainstay to protect cardias 2. Reduce hyperthermia a. Cooling blanket and antipyretic b. Aspirin are contraindicated because they inhibit protein binding T3 and T4 increasing the level of free metabolically active thyroid hormone 3. Fluid Replacement a. Vigorous fluid replacement must be instituted to treat or prevent dehydration b. Antibiotic therapy may be warranted for infection c. Large volumes of glucose and isotonic sodium solutions 4. Pharmacologic Management - Beta blocker are administered to decrease the peripheral cellular sensitivity to catecholamines - Antithyroid meds to block the synthesis and release of thyroid hormone into circulation and to inhibit peripheral conversion of T4 to T3 a. Medications that block catecholamine effect i. Beta-adrenergic blocking agents are used to decrease the catecholamine effects ii. Have no effect on thyroid hormone but reduce exaggerated myocardial stimulation ands slow av conduction rate iii. Propranolol (oral) or esmolol iv. Verapamil and diltiazem may be used to lower HR in pt who cannot take beta-blockers v. Beta blocker represent first line emergency treatment b. Medications that block thyroid synthesis i. Propylthiouracila and methimazole ii. iii. Via mouth or tubing tube Propylthiouracil is especially therapeutic because it blocks conversion of t4 to t3 iv. Methimazole has a slower rate of action but it's more potent than PTU v. Both medications act within 1 to 2 hours after absorption from gastrointestinal tract c. Medications that block release of Thyroid hormone i. Inorganic iodine blocks the release of any formed thyroxine that is already in the thyroid gland but not yet released ii. Given 1 hour after administration of the antithyroid synthesis to prevent iodide from being used for thyroid hormone production iii. Hydrocortisone and dexamethasone given to pt wt adrenal insufficiency during initial thyroid storm Nursing Management 1. Medication Administration a. Hr should decrease with beta-blockade b. Agitation is normal and decreases with medication 2. Normalize Body Temperature a. Temperature is assessed frequently until normal body temp is attained b. Cool environment and a fan to circulate air c. Tepid sponge bath d. Cold pack applications to grain and axilla e. Avoid salicylates 3. Rehydration and Correction of Metabolic Derangements a. Fluids and electrolytes replacement b. Glucose solution are given to replace glycogen stores, which are depleted c. Insulin administration to treat hyperglycemia d. Hyponatremia treated with isotonic iv fluid replacement 4. Patient education a. Beta blocker side effect bradycardia, unexplained fatigue, orthostatic hypotension b. Antithyroid meds side effect- agranulocytosis sudden cough,fever, rash and inflammation 28. SIADH: complications, nursing interventions, signs and symptoms, assessment - Dilutional hyponatremia Excess of ADH secreted Excessive adh stimulates kidneys to retain fluid - Excessive adh alters sodium balance in extravascular Aldosterone production is suppressed Assessment - Edema usually not present - Slight weight gain - Lethargy, anorexia, nausea and vomiting - Severe neurological symptoms if less sodium less than 120 mEq/L (mental confusion, apprehension, seizures. Altered loc, coma and death) - Hyponatremia, concentrated urine - Decrease plasma osmolality less than 276 mOsm/kg H20 - Increase urine osmolality more than 100 mOsm/kg H20 - Urine sodium concentration elevated greater than 40 mEq/L - Copeptin is a biomarker for ADH Medical Management - Fluid restriction is the cornerstone. Restricted to 500 to 1000mL/day - Too rapid sodium correction must be avoided to reduce osmotic demyelination (white matter of the brain) - Increase sodium slowly by 8 mEq/L in 24 hrs - Sodium evaluated every 4 hours - Sodium should not be increase 10 mEq/L in 24 hrs - Slow infusion of 3% saline (hypertonic saline) used to - - replenish serum sodium without adding extra volume Vaptans - increase the action of ADH on the V1 kidney tubule receptors so more water is excreted Vasopressin receptor antagonists used to treat euvolemic hyponatremia Nursing Interventions - Fluid restriction - Assessment of fluid - Measurement of I&O - Daily weight - Oral care Complications - Hyponatremia BONUS? TYPES OF DIURETICS 1) THIAZIDE DIURETICS: Mechanism: Act on the distal convoluted tubule of the kidney to inhibit sodium reabsorption, leading to increased excretion of sodium and water. Examples: Hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide. 2) LOOP DIURETICS: Mechanism: Act on the ascending loop of Henle in the kidney to inhibit sodium-potassium-chloride cotransporter, resulting in increased excretion of sodium, potassium, and water. Examples: Furosemide (Lasix), Bumetanide, Torsemide. 3) POTASSIUM-SPARING DIURETICS: Mechanism: Act on the distal convoluted tubule and collecting ducts to block the action of aldosterone, thereby promoting sodium excretion while conserving potassium. Examples: Spironolactone, Eplerenone, Amiloride, Triamterene. 4) OSMOTIC DIURETICS: Mechanism: Non-absorbable substances that increase the osmotic pressure in the renal tubules, inhibiting water reabsorption and leading to increased urine production. Examples: Mannitol, Urea. 5) CARBONIC-ANHYDRASE INHIBITORS: Mechanism: Inhibit the enzyme carbonic anhydrase in the proximal convoluted tubule, reducing bicarbonate reabsorption and increasing excretion of sodium, potassium, and bicarbonate. Examples: Acetazolamide.