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FLUID AND ELECTROLYTE IMBALANCE DR. JENNIFER TAYLOR, PHD, RN, CNE NURS 201 – PATHOPHYSIOLOGY FOR NURSING PRACTICE BODY FLUID 60% of human body is fluid:...

FLUID AND ELECTROLYTE IMBALANCE DR. JENNIFER TAYLOR, PHD, RN, CNE NURS 201 – PATHOPHYSIOLOGY FOR NURSING PRACTICE BODY FLUID 60% of human body is fluid:  Average: 42 L total body fluid (mostly water)  Majority component in cells, bloodstream  Solvent for body solutes/electrolytes Fluid compartments:  Fluid constantly shifts between compartments  ICF: Intracellular fluid (within cells)  40% total body weight, typically most stable  ECF: Extracellular fluid (blood stream)  20% total body weight, IVF (intravascular fluid)  ISF: Interstitial fluid (between cells, tissue) Image Credit: Image Credit: https://doctorlib.info/physiology/physiology-2/52.html https://slideplayer.com/slide/10873065/ BODY FLUID BALANCE, MOVEMENT Homeostasis Goal = balance/equilibrium of solute and water Diffusion: passive across membrane  substance/electrolyte Osmosis: passive moves from high to low  water moves from high to low water concentration concentration  Semi-permeable membrane selectively limits size of solute molecules (i.e. proteins (albumin) too large) BODY FLUID BALANCE, MOVEMENT Facilitated transport: active Active transport: active  Energy required to move substance across  Carrier proteins carry molecules through plasma membrane membrane against gradient  Ex: Na+/K+ pump balances K+ ICF, Na+  Ex: glucose facilitated by carrier protein insulin; ECF large glucose molecule needs facilitation BODY FLUID BALANCE, MOVEMENT Homeostasis: Hydrostatic pressure = Osmotic pressure  Goal: maintain equilibrium between body fluid (water) and solutes (electrolytes, proteins)  Fluid shifts when pressures create unequal balance across cell membrane Starling’s Law of Capillary Forces: osmotic & hydrostatic pressure in balance/opposition  Osmotic pressure > Hydrostatic pressure, more fluid shifts to ICF (cellular swelling/edema)  Hydrostatic pressure > osmotic pressure, more fluid shifts to ECF (cellular dehydration) Hydrostatic pressure: water pushes (osmosis)  Water pushes into cell from vessels (high to low pressure)  Force shifts fluid from ECF (vessels) to ICF (cells) HOMEOSTASIS INTERRUPTED…. Body fluid level imbalance:  Fluid > or < “normal” inhibits body functions Body fluid functions:  Universal biologic solvent (all chemical reactions occur in medium of water)  Regulate electrolyte distribution in ECF, ICF  Transport hormones, nutrients  Dilute & transport toxins, waste products  Transport O2 to cells, CO2 to lungs  Modulate temperature shifts; absorb heat w/out changing temperature Image Credit: http://humanbiologylab.pbworks.com/w/page/50150566/Water BODY FLUID HOMEOSTASIS Fluid Homeostasis: balance of fluid intake & output  Osmolarity (solute levels in fluid) is body mechanism to monitor/assess body fluid status Mechanisms to maintain fluid homeostasis:  Triggered by hypothalamus when osmolarity is high (low fluid)  Thirst: conscious desire to drink (increase intake)  ADH (anti-diuretic hormone): body retains fluid, reduces output  Released by posterior pituitary  Opposite of diuresis (excess production of urine)  RAAS: renin-angiotensin-aldosterone system Image Credit: https://careclinic.io/track-water-intake/  Natriuretic peptides: excrete sodium & water BODY FLUID HOMEOSTASIS Renin-Angiotensin-Aldosterone System (RAAS) Hypotension, hypovolemia, low cardiac output (CO)  Low fluid volume, low BP -> fluid retention  Low circulating fluid -> reduced renal perfusion  Kidneys release renin (starts RAAS compensation)  Renin converts angiotensin (from liver) to angiotensin 1  ACE (lungs) converts angiotensin 1 to angiotensin 2 (powerful vasoconstrictor), vasoconstriction increases blood pressure (BP)  Triggers adrenal glands to release aldosterone (fluid retention)  Aldosterone increases reabsorption of Na+, retention of Na + water  Increased BP & fluid retention = return to normal blood volume FLUID IMBALANCES: EDEMA Edema: swelling produced by increase in ISF and/or ICF  ISF: can hold 10 – 30 L of additional fluid  Pitting edema: exceed tissue absorption capacity, displace tissue  Dependent edema = gravity related (typically LE)  Nonpitting edema = firm, accumulation of plasma proteins Image Credit: (inflammation) https://www.mayoclinic.org/diseases- conditions/edema/symptoms-causes/syc- Etiology (cause): 20366493  High hydrostatic pressure: excess fluid in bloodstream  Sodium retention: Na+ triggers dehydration/thirst  Ex: fluid accumulates in lungs (heart failure), fluid shift to alveoli  Low osmotic pressure: low solutes to hold fluid in vessels  Ex: hypoalbuminemia (low albumin) w/poor protein intake  Inflammation, injury: inflammatory response increases capillary permeability, fluid shifts (swelling) FLUID IMBALANCES: EDEMA Assessment:  Symptoms determined by edema location  Impaired movement, function (swelling)  Increased extremity circumference  Weight gain: 1 L fluid = 2.2 pounds  Decreased blood flow (hypoxia)  Wounds/ulcerations: skin susceptible to injury Life-threatening edema:  Brain (cerebral edema), lungs (pulmonary edema), larynx (laryngeal edema) Image Credit: http://www.med-health.net/Edema-Grading.html FLUID IMBALANCES: HYPERVOLEMIA Excess fluid in body (overhydration), fluid volume overload Etiology (causes):  High hydrostatic pressure (too much ECF), fluid shifts into ICF  Excess sodium: increased fluid retention  Ex: Heart failure – poor cardiac output stimulates RAAS, excess ECF in vessels, results in FVO  Excess ADH: excess retention of fluid (lack of diuresis)  Ex: SIADH - dilutional hyponatremia (fluid retained, Na+ concentration/osmolarity falls)  Ex: cirrhosis of liver - stimulates ADH release, impairs blood flow through the liver & fluid accumulates (ascites) Image Credit: https://training.seer.cancer.gov/anatomy/cardiovascular/blood/physiology.ht FLUID IMBALANCES: HYPERVOLEMIA Assessment:  CV: HIGH CARDIAC VOLUME (circulatory overload)  Hypertension (HTN)  Peripheral edema (pressure shifts fluid)  Bounding pulse (vessels FULL), elevated arterial and venous pressure (HTN)  Resp: dyspnea, pulmonary congestion (fluid), crackles, cough  Pressure shifts fluid into lung tissue  Skin: dry, shiny, stretched/“tight” w/edema Image Credit: https://www.fluidacademy.org/blog- foam/item/global-increased-permeability-syndrome-  General: weight gain (acute) isicem18-ifad2018.html FLUID IMBALANCES: HYPOVOLEMIA Diminished fluid in body/bloodstream (dehydration), fluid volume deficit  Decreased blood volume, impairs cardiac function Etiology (causes):  Reduced fluid intake and/or excess fluid loss  Ex: burn injuries, perspiration, diarrhea, vomiting, etc.  High osmotic pressure, fluid shifts into from ICF to ECF  Ex: uncontrolled diabetes mellitus (DM) – excess glucose in blood (high osmolarity), osmotic pressure draws fluid out of cells into ECF -> cellular dehydration  Insufficient ADH: excess fluid loss (diuresis, excess urination)  Ex: Diabetes insipidus (DI) - hypernatremia (fluid lost, Na+ retained, osmolarity rises) Complication: renal dysfunction related to decreased excretion of waste products FLUID IMBALANCES: HYPOVOLEMIA Assessment:  CV: LOW CARDIAC VOLUME  Hypotension (esp w/standing)  Tachycardia: elev HR to compensate low BP  Reduced peripheral perfusion  Weak/thready pulse (vessels EMPTY), decreased arterial and venous pressure  Neuro: dizzy, weak, LOC changes  HA (poor cerebral blood/oxygen supply)  Renal: Urine output ↓ (< 30 ml/hr)  Concentration ↑ (dark yellow, high S.G.)  Skin: dry skin/mucous membranes, turgor  General: thirst, weight loss (acute) ELECTROLYTES Electrolytes:  charged ions (cation+, anion (-))  Essential to metabolism, energy production  Cell function (esp. nerve & muscle cells)  Impulse conduction (action potential), muscle contraction  Na+, K+ primary role in cell depolarization & repolarization Solutes: substances dissolved in ICF & ECF Protein molecules: essential body solute  Maintains fluid balance, prevents shift of fluid  Transports substances throughout body ELECTROLYTE BALANCE Normal Electrolyte Concentratio n 135 – 145 Sodium (Na++) ECF mEq/L 3.5 – 5.0 Potassium (K+) ICF mEq/L 8.7 – 10.5 Calcium (Ca++) ECF mg/dL 98 – 106 Chloride (Cl-) ECF mEq/L Image Credit: https://www.researchgate.net/figure/onic- Magnesium 1.5 – 2.5 concentration-of-both-intracellular-and-extracellular-fluids- ICF Image-source_fig3_309522864 ELECTROLYTE BALANCE, MOVEMENT Osmotic pressure: electrolytes/solutes (proteins) pull  Pressure exerted by increased concentration of solutes  Pull water from cells (diffusion)  High concentration to low concentration  Pressure shifts water from ICF to ECF (vessels), balance/equalize concentration in vessels Osmolarity: solutes/liter of body fluid  Number of electrolyte particles in fluid  High serum osmolarity = excess electrolyte in blood  Low serum osmolarity = reduced electrolyte in blood Image Credit: https://biology.stackexchange.com/questions/40883/osmolarity-vs- ELECTROLYTE BALANCE, MOVEMENT Tonicity:  Osmotic pressure Isotonic: osmotic pressure = to body fluids difference between two  No fluid movement across membrane solutions Hypotonic: osmotic pressure < body fluids  Ex: Intravenous (IV) fluids  Low osmolarity, low solute concentration per liter  Fluid/water moves into cell, cell edema (swells) Hypertonic: osmotic pressure > body fluids  High osmolarity, high solute concentration per liter  Fluid/water moves out of cell, cell dehydration (shrinks) Image Credit: Tonicity concepts essential to understanding IVF https://2012books.lardbucket.org/books/an-introduction- to-nutrition/s11-01-overview-of-fluid-and-electrol.html solutions SODIUM (NA+) Sodium Normal Range = 135 – 145 mEq/L  Sodium 90% of ECF cations  Imbalance: Hyponatremia - Serum Na++ < 135 mEq/ml  Imbalance: Hypernatremia - Serum Na++ > 145 mEq/ml Primary role: fluid volume balance  Elevated Na+ = fluid retention Other Na+ functions:  Nerve impulse conduction  Critical to muscle contraction  Facilitates membrane transport (Na+/K+ pump) Image Credit: https://content.openclass.com/eps/pearson- reader/api/item SODIUM & BODY FLUID Wherever Sodium Goes, Water Will Follow  Fluid imbalances linked to sodium imbalances  Sodium (Na+) major ECF cation, regulates ECF volume  Na+ levels accounts for majority of osmotic activity (body fluid/water movement) Hyponatremia: low Na+ osmolarity  Low ECF concentration of Na+ shifts fluid from ECF to ICF (cellular edema) Hypernatremia: high Na+ osmolarity  High ECF concentration of Na+ shifts fluid from ICF to ECF (cellular dehydration) Image Credit: https://nursekey.com/hyponatraemia-and-its-prevention/ SODIUM IMBALANCE Severe Na imbalance most dramatic impact to brain due to effect on cerebral fluid balance (or imbalance….) Image Credit: https://link.springer.com/article/10.1186/s13049-019- ELECTROLYTE IMBALANCE: HYPONATREMIA HYPERVOLEMIC Hyponatremia Etiology: Hypervolemic causes  Fluid overload dilutes Na+: renal failure, heart failure  Excess fluid most common cause of hyponatremia  SIADH (Syndrome of Inappropriate ADH) Assessment: symptoms manifest < 125 mEq/ml  Symptoms related to hypervolemia & hyponatremia/cell edema  Neuro/MS: HA, confusion, weakness, fatigue, muscle cramps  Severe (r/t cerebral edema): lethargy, seizure, coma, death Image Credit:  CV (excess volume): HTN, bounding pulse https://5minuteconsult.com/collectionco ntent/1-151755/diseases-and-  GI (excess volume, ascites): nausea, vomiting, diarrhea conditions/hyponatremia ELECTROLYTE IMBALANCE: HYPONATREMIA HYPOVOLEMIC Hyponatremia Etiology: Hypovolemic causes  Renal loss: diuretics, renal disease (excess Na excretion)  Non-renal: loss of sodium & fluid  Ex: vomiting, GI suctioning, wound drainage, sweating, burns, etc. Assessment: symptoms manifest < 125 mEq/ml  Symptoms related to hypovolemia & hyponatremia/cell edema  Neuro/MS: HA, confusion, weakness, fatigue, muscle cramps  Severe (r/t cerebral edema): lethargy, seizure, coma, death  CV (hypovolemia): Tachycardia, hypoTN (low BP esp w/standing)  Renal: low urine output (oliguria), azotemia (excess waste in blood)  General (hypovolemia): thirst, poor skin turgor, dry mucosa Image Credit: ELECTROLYTE IMBALANCE: HYPERNATREMIA HYPOVOLEMIC Hypernatremia Etiology: Hypovolemic causes  Excess fluid loss most common cause (fluid lost, Na left behind)  Fever, watery diarrhea, tachypnea, etc.  Decreased water intake (esp w/elderly)  DI: Na+ retention, excretion of excess dilute urine Assessment: symptoms manifest > 155 mEq/ml  Symptoms r/t cellular dehydration (Excess Na ECF pulls water from ICF)  Neuro: restless, irritable, muscle twitching/spasms  Severe (r/t cerebral dehydration): lethargy, seizure, coma, death  CV (hypovolemia): Tachycardia, hypoTN  General (hypovolemia): thirst, fever Image Credit: https://slideplayer.com/slide/10431894/ ELECTROLYTE IMBALANCE: HYPERNATREMIA HYPERVOLEMIC Hypernatremia Etiology: Hypervolemic causes  Hyperaldosteronism – increase tubular reabsorption  Excess salt intake, Antacids with sodium bicarbs Assessment: symptoms manifest > 155 mEq/ml  Symptoms r/t cellular dehydration (Excess Na ECF pulls water from ICF)  Neuro: restless, irritable, muscle twitching/spasms, severe (r/t cerebral dehydration): seizure, coma, death  CV (hypervolemia): Tachycardia, hyperTN, bounding pulse  Resp (hypervolemia): dyspnea, pulmonary congestion  General (hypervolemia): weight gain Image Credit: https://emcrit.org/wp-content/uploads/2016/11/Hyp ernatremia-in-Critically-Ill-Pts.pdf POTASSIUM (K+) Potassium Normal Range = 3.5 – 5 mEq/L  Primary cation in ICF (cell is “OK”), 2% in plasma (ECF)  Hypokalemia - Serum K+ < 3.5 mEq/ml  Hyperkalemia - Serum K+ > 5 mEq/ml Primary role: Maintain action potentials  K+ gradient stimulus for action potential initiation (electrical excitability) Image Credit:  K out, Na in = cell depolarization (cardiac rhythms, muscle contraction) https://www.differencebetwee n.com/difference-between- depolarization-and-vs- Other functions: repolarization/  Acid-base balance: hydrogen, K+ shifts b/t ICF & ECF to maintain pH Potassium Regulation: nephrons (kidney), aldosterone triggers K+ excretion POTASSIUM & PH Intracellular pH Buffer:  H+ and K+ ion exchange, shift between ICF and ECF to buffer pH Alkalosis (high pH): H+ moves out Acidosis (low pH): H+ moves into of cell, K+ into cell (hypokalemia) cell, K+ moves out (hyperkalemia) Image Credit: http://notezonnursing.blogspot.com/2011/05/some- ELECTROLYTE IMBALANCE: HYPOKALEMIA Etiology:  Excess K+ excretion (renal)  Medication side effects (diuretics most common cause)  Severe GI loss: vomiting, diarrhea  Inadequate intake of K+  Ex: NPO status, bariatric surgery  Alkalosis: ECF K+ shifts into ICF, H+ ions shift out Image Credit: https://study.com/academy/lesson/what-is- Assessment: Decreases cell excitability, action hypokalemia-definition-causes-symptoms-treatment.html potential  CV: hypoTN (low BP esp w/standing), cardiac arrythmias  Prolonged PR interval (delayed conduction atria to ventricles)  Flattened T wave (decreased repolarization/action potential) Image Credit: https://www.nclexquiz.com/blog/ecg-ekg-changes-  Neuro/MS: muscle fatigue, weakness, leg cramps, hypokalemia-hyperkalemia/ ELECTROLYTE IMBALANCE: HYPERKALEMIA Etiology:  Excess K+ retention/decreased K+ excretion (renal)  Renal failure (most common)  Massive injury/burn (releases K+ from damaged cells)  Acidosis: ICF K+ shifts into ECF, H+ ions shift into cell Assessment: increases excitability, action potential Image Credit: https://study.com/academy/lesson/what-is- hypokalemia-definition-causes-symptoms-treatment.html  Decreases excitability threshold (fires too quick)  Levels > 7.0 mEq/L significant, Levels > 8.5 mEq/L fatal  CV: Ventricular dysrhythmias (v-fib, cardiac arrest)  Peaked T wave (excess repolarization)  Wide QRS interval (impaired ventricular Image Credit: https://www.nclexquiz.com/blog/ecg-ekg-changes- conduction) hypokalemia-hyperkalemia/ CALCIUM (CA++) Calcium Normal Range = 8.7 – 10 mg/dL  99% of Ca+ bound in bones, teeth (primary mineral)  1% in circulation, ECF (measure serum levels)  Hypocalcemia - Serum Ca++ < 8.7 mg/dL  Hypercalcemia - Serum Ca++ > 10 mg/dL Serum (free) calcium functions:  Neuro: nerve impulse conduction/excitability, muscle contraction  Blood clotting factor Regulation of Calcium: parathyroid hormone (PTH) Image Credit: https://ascientificcuriosity.wordpress.com/health- and-nutrition/calcium-got-plants/  Decreased serum calcium concentration stimulates PTH, mobilizes calcium in bones to stabilize serum calcium ELECTROLYTE IMBALANCE: HYPOCALCEMIA Etiology:  Insufficient supply of calcium (most common)  Inadequate calcium or Vitamin D intake Chvostek’s sign:  Hypoparathyroidism: inability to get Ca from facial nerve twitch w/light tap to facial bone nerve  Increased excretion of calcium  Renal disease, diarrhea, wound drainage Assessment: Increased neural excitability (fire more easily)  Neuro: muscle twitch/cramps, tetany (contraction), hyperreflexia, paresthesia (numbness, tingling)  CV: HypoTN, arrhythmias Trousseau’s sign: carpopedal spasm w/blood  Resp: dyspnea, laryngospasm flow occlusion (Ca++ concentration produces ELECTROLYTE IMBALANCE: HYPERCALCEMIA Etiology:  Increased calcium from bone  Metastatic Cancer (most common cause): Ca++ released from bone destroyed by cancer  Immobility: increased Ca from bone loss  Hyperparathyroidism: excess PTH increases Ca from bone  Excessive calcium or Vitamin D intake Assessment: Decreased neural excitability (less able to fire)  Neuro: muscle weakness, hyporeflexia/ataxia (flaccid/limp), paresthesia (numbness, tingling) “Bones, Stones, Groans,  CV: HyperTN, arrhythmias Moans” Image Credit:  MS: osteopenia (bone loss), bone pain, https://www.slideshare.net/DrLalaSho uravDas/hypercalcemia-82719827 pathologic Fx PHOSPHORUS Phosphorus Normal Range = 2.5 – 4.5 mg/dL  ICF anion (14% in cells), 85% of phosphorus in bones  Hypophosphatemia, Serum Phosphorus < 2.5 mg/dL  Hyperphosphatemia, Serum Phosphorus > 4.5 mg/dL Roles of Phosphorus:  Formation of teeth and bones, red blood cells  Essential to carb, protein, lipid metabolism, ATP creation  Building block of nucleic acids (RNA & DNA)  Regulate acid-base as buffer Image Credit: Regulation of Phosphorus: https://sites.google.com/site/faiqyosefchem10h p2/role-of-phosphorus-in-the-body?tmpl=  Renal: Phosphate excretion depends on serum phosphate concentrations %2Fsystem%2Fapp%2Ftemplates%2Fprint %2F&showPrintDialog=1  PTH: elevated PTH reduces phosphate retention (inverse relationship)  Reciprocal to calcium regulation to prevent Ca++ phosphate crystals HYPOPHOSPHATEMIA & HYPERPHOSPHATEMIA Hypophosphatemia Hyperphosphatemia Serum Phosphorus < 2.5 mg/dL Serum Phosphorus > 4.5 mg/dL Etiology Decreased intestinal absorption Renal failure (reduced secretion) (diarrhea, prolonged antacids, low Rhabdomyolysis (rapid production) Vit D) Malnutrition, alcoholism Increased renal loss, alkalosis Assessmen Decrease energy, deficiency in ATP S/S related to complementary t Neuro: tremors, paresthesia, calcium deficit weakness, hyporelexia, confusion, Neuro: Paresthesia, tetany stupor, coma CV: Hypotension, arrhythmias MS: weak, joint stiffness, bone pain Blood: Hemolytic anemia (hemolysis), impaired WBC & MAGNESIUM Magnesium Normal Range = 1.5 – 2.5 mg/dL  ICF cation, majority stored in bone (60%)  Hypomagnesemia – serum magnesium < 1.5 mg/dL Image Credit: http://drleonardcoldwell.com/why-  Hypermagnesemia – serum magnesium > 2.5 mg/dL magnesium-is-the-most-essential- mineral-your-body-isnt-getting- enough-of/ Roles of Magnesium:  Essential for absorption of Calcium & Vitamin D (necessary for PTH function)  Co-factor in enzymatic reactions (over 300, esp carb & protein metabolism)  Facilitates ATP production (powers Na-K pump)  Transmits electrical impulse across nerves/muscle via K+ & Na+ channels Regulation of Magnesium:  Renal, GI system balance through selective absorption, excretion  PTH stimulates magnesium reabsorption (triggered by Ca++ levels) HYPOMAGNESEMIA & HYPERMAGNESEMIA Hypomagnesemia Hypermagnesemia Serum Magnesium < 1.5 mg/dL Serum Magnesium > 2.5 mg/dL Increased excretion/loss of magnesium Decreased excretion of magnesium (GI loss, renal disease) (renal disease, kidney injury, Etiology Insufficient supply of magnesium untreated DKA) (malnutrition, malabsorption, alcohol VERY rare; kidneys very effective at abuse) regulating high magnesium VERY SIMILAR TO HYPOCALCEMIA S/S related to neuromuscular and CV (hypomagnesemia common cause d/t function PTH) Neuro: hyporeflexia, muscle Neuro: hyperreflexia, tremors, weakness, drowsiness Assessm nystagmus (eye twitch), irritability, CV: HypoTN, tachycardia shifting to ent anxiety, mood changes bradycardia, prolonged PR, Positive Chvostek & Trousseau signs widened/delayed QRS, peaked T CV: tachycardia, HyperTN, cardiac CHLORIDE Chloride Normal Range = 98 – 106 mEq/L  ECF anion, majority stored in bone (60%)  Hypochloremia – serum chloride < 98 mEq/L  Hyperchloremia – serum chloride > 106 mEq/L Roles of Chloride:  Essential for regulation of fluid (BP), pH balance  Supports nerve impulse conduction, muscle contraction  Facilitates absorption of nutrients  Bound to Na+, tend to fluctuate similarly Regulation of Chloride:  Renal balances through selective absorption, excretion Image Credit: https://www.eufic.org/en/vitamins-and-minerals/article/chloride- foods-functions-how-much-do-you-need-more HYPOCHLOREMIA & HYPERCHLOREMIA Hypochloremia Hyperchloremia Serum Chloride < 98 mEq/L Serum Chloride > 106 mEq/L Increased excretion/loss of chloride (GI VERY rare loss, renal disease, excess sweating) Dehydration: medications (diuretics), pH imbalance: Chronic respiratory heat exposure, decreased fluid intake Etiology acidosis, metabolic alkalosis Decreased excretion of chloride (renal Rare – typically only impacts critical disease) care/ICU Typically occurs w/Hyponatremia Typically occurs w/Hypernatremia No direct symptoms Fluid retention: HTN, edema Assessm Symptoms reflect associated CV: impaired conduction, irregular HR ent imbalances of other electrolyte Neuro: weakness, confusion disorders or cause REFERENCES  Mosby’s Dictionary of Medical, Nursing & Health Professions. (2009). (8th Ed.). St. Louis, MO: Mosby Elsevier.  Capriotti, T. (2024). Davis Advantage for pathophysiology: Introductory concepts and clinical perspectives (3rd Ed.). FA Davis: Philadelphia, PA.

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