Nephro final

What is the urine output rate for an anuric patient

less than 50 milliliters per day

What is the urine output rate for an oliguric patient

< 500 milliliters per day

What is the urine output rate for a non oliguric patient

> 500 ml/day

What are some limitations in staging AKI?

Biomarkers of Scr and urine output have limitations Scr ----Lag in SCr rise (48-72 hours from time of injury) ----Baseline SCr must be known Urine Output ----Non-specific marker ----Depends on volume, diuretic use and cause of AKI

What are some risk factors for AKI

Age volume status Comorbid conditions (CKD, DM, HTN, CAD, CHF, Liver) Proteinuria Medication and nephrotoxic exposure Surgery Sepsis

What are some causes of prerenal AKI

Volume Depletion Decreased Cardiac Output Functional (NSAIDS, ACEI)

What are some factors that may lead to pre-renal AKI caused by dehydration?

Hemorrhage Decreased effective perfusion volume (nephrotic syndrome, cirrhosis, edema) Vasodilation (sepsis) Diuretics Thirst, hypotension, tachycardia

What are some factors that may lead to pre-renal AKI caused by decreased cardiac output?

Congestive heart failure Myocardial infarction Cardiac surgery

Desribe the lab values that would indicate pre-renal AKI

Urine sodium < 20 Urine osmolality : serum osmolality > 1.5 BUN : Scr > 20 Low fractional excretion of sodium (FeNa) (Pre-renal failure: <1%)

What is the treatment goal for prerenal AKI management

restore renal blood flow by increasing intravascular volume

what is the treatment for prerenal AKI when it is caused by hemorrhage

Packed red blood cells

what is the treatment for pre renal AKI when it is caused by plasma losses (burns) or volume loss

Crystalloids or colloids solutions

what is the treatment for pre renal AKI when it is caused by decreased cardiac output

Positive inotropes, Vasopressors, intra-aortic balloon pump

What is the cause of the majority of cases intrinsic AKI

acute tubular necrosis

Fill in the blank: Tubules highly susceptible to _______ damage

Ischemic

What are some nephrotoxins that may cause ATN

Antibiotics Chemotherapy Contrast Many more

What can cause renal hypoperfusion?

Hypovolemic states Low cardiac output Sepsis

What are some causes of ATN

nephrotoxins, renal hypoperfusion

What are the four phases of ATN

1) Initiation --Renal tubular epithelial cell injury (vasoconstriction and ischemia) --Lead to GFR reduction 2)Extension --Continued cell injury and inflammatory response 3)Maintenance --GFR reaches lowest point --Initial recovery of kidneys 4)Recovery --New tubule cells are regenerated

What are some lab results that indicate ATN

Color and appearance: muddy brown (RBC and WBC Casts) Granular or epithelial cell casts Urine : serum osmolality < 1.3 BUN : Scr ≈ 15 FeNa >2%

Hhow do you manage ATN

Improve urine output Restore kidney function Improve survival

What are some causes of post renal AKI

Bladder Outlet obstruction (BPH, cancer, surgery) Ureteral obstruction (Nephrolithiasis)

What are some lab results that indicate post renal AKI

Urine sodium> 40 BUN : Scr ratio ≈ 15 Some cellular debris in urine Urine : serum osmolality < 1.5 FeNa: Variable

How do you manage post renal AKI

Removal of obstruction Pharmacological: alpha1 blockers for BPH Catheterization Percutaneous nephrostomy

What are some complications of AKI

Volume overload and edema Electrolyte imbalance Acid Base disorder Malnutrition Drug dosage adjustment

What does the in general management of AKI look like?

Supportive care Maintaining hemodynamic stability Fluid and electrolyte management Maintain renal perfusion Eliminate nephrotoxins (if feasible), drug dosing Renal Replacement Therapy (RRT)

What are the two forms of renal replacement therapy

intermittent hemodialysis (IHD) continuous renal replacement therapy (CRRT)

describe intermittent hemodialysis

Short treatment session (3 to 4 hours) Rapid removal of volume and small solutes Can cause hypotension

Describe continuous renal replacement therapy

Reserved for unstable patients More solute removal Less hypotension risk

Describe the clinical presentation of volume overload

peripheral and pulmonary edema

Describe the management of volume overload

Fluid Restriction/Limit sodium intake Loop Diuretics (Careful in AKI, increased mortality..Diuretic resistance)

Why is there diuretic resistance in volume overload

Bioavailability reduced

What are some methods to improve diuretics efficacy when dealing with diuretic resistance in volume overload

Continuous instead of intermittent (More consistent concentration) Combination therapy (use loops with another diuretic that works at distal tubule)

What are some important considerations when dosing in AKI

Pharmacokinetic alterations Estimate of renal function Vd (drug’s normal Vd and patient’s volume status) Type of RRT Drug monitoring/Therapeutic window Individualized approach

What are some risk factors for drug induced kidney disease

Advanced age (>70) Male Gender African American Race Pre-existing renal disease Diabetes Heart Failure Presence of other nephrotoxic drugs Sepsis Volume depletion Cirrhosis Surgery Shock Acidosis Dose, duration, & frequency of toxins

What are some drugs that can cause prerenal acute renal failure

NSAIDS ACEI/ARB SGLT-2s inhibitors Diuretics Cyclosporine Tacrolimus

Describe the presentation of ACEI/ARB Nephropathy

Acutely reduce GFR Moderate rise in Scr up to 30% common after initiation Scr stabilizes within 1 to 2 weeks

What are some methods to prevent ACEI/ARB Nephropathy

Recognize risk factors Initiate at low doses and gradually titrate (every 2 to 4 weeks) Monitor Scr and potassium frequently Avoiding other nephrotoxic drugs if possible

Describe the management of ACEI/ARB Nephropathy

Scr threshold for discontinuation not in guidelines Scr increase (<30%) – continue and repeat labs in 1-2 weeks Scr increase from 30 to 50% - decrease the dose by half and repeat labs Scr increase by >50% - discontinue ACE/ARB Renal damage reversible upon discontinuation

What is the incidence of NSAID nephropathy

500,000 to 2.5 million people annually

Describe the mechanism of NSAID nephropathy

Ischemic kidney damage Decreased synthesis of renal vasodilator Afferent vasoconstriction Result in reduced renal perfusion and pressure

What are some risk factors for NSAID nephropathy

Age > 60 Pre-existing kidney disease Hepatic disease CHF Volume depletion Lupus Concurrent treatment with ACEI/ARB or diuretics –avoid in high risk

Describe the clinical presentation of NSAID nephropathy

Occur within 2 to 7 days after initiation Diminished urine output, weight gain, edema Elevated Scr, potassium and BP

Describe the prevention of NSAID nephropathy

Avoiding use in high-risk patients (If necessary, minimal effective dose for shortest duration) Maintain adequate hydration

Describe the treatment of NSAID nephropathy

Discontinuation of offending agent and other nephrotoxic drugs Reversible, recovery within 3 to 5 days Rare cases of chronic renal failure

Etodolac brand

Lodine

Lodine generic

Etodolac

Nabumatone brand

Relafen

Relafen generic

Nabumatone

Sulindac brand

Clinoril

Clinoril generic

Sulindac

Describe the presentation of tacrolimus nephropathy

Occurs within days of initiation Rise in Scr HTN Hyperkalemia Sodium retention Renal tubular acidosis Hypomagnesemia

escribe the presentation of cyclosporine nephropathy

Occurs within days of initiation Rise in Scr HTN Hyperkalemia Sodium retention Renal tubular acidosis Hypomagnesemia

Describe the prevention of tacrolimus nephropathy

PD and PK monitoring Decreased doses when used with other non-nephrotoxic immunosuppressants

Describe the prevention of cyclosporine nephropathy

PD and PK monitoring Decreased doses when used with other non-nephrotoxic immunosuppressants

Describe the treatment of tacrolimus nephropathy

Acute injury: dose related and improves with dose reduction or discontinuation of interacting meds Chronic kidney injury: not dose related and irreversible

Describe the treatment of Cyclosporine nephropathy

Acute injury: dose related and improves with dose reduction or discontinuation of interacting meds Chronic kidney injury: not dose related and irreversible

Which SGLT 2 inhibitors have some evidence to show that they can induce acute kidney injury

Canagliflozin and dapagliflozin

What is the incidence of SGLT 2 inhibitor nephropathy

over 100 cases reported to the FDA

describe the mechanism of SGLT 2 inhibitor nephropathy

Osmotic diuresis that leads to volume depletion Delivery of sodium chloride vasoconstricts afferent arterioles and reduce GFR

What are some risk factors for SGLT 2 inhibitor nephropathy

Older age Concomitant nephrotoxic medication (ACEI/ARB, diuretics, NSAIDS) Volume depletion

Describe the prevention of SGLT 2 inhibitor nephropathy

Close follow-up in patients taking ACEI/ARB and diuretics Avoiding nephrotoxins

Describe the management of SGLT 2 inhibitor nephropathy

Discontinuing SGLT-2 allows kidney recovery If volume depletion – IV fluids If ATN develops – supportive care (RRT) SGLT-2s can be restarted when kidney recovers

Rank the aminoglycosides in order from most to least likely to cause nephrotoxicity

Neomycin>gentamicin>tobramycin>amikacin

Describe why some aminoglycosides are more nephrotoxic than others

Toxicity related to cationic charge of the drug. The more cationic, the more likely to create reactive oxygen species

what are some risk factors for aminoglycoside nephrotoxicity

aggressiveness dosing, synergistic toxicity from combination, and pre-existing clinical conditions

Describe the prevention of aminoglycoside nephrotoxicity

selection of patient, alternative agents when possible, avoid volume depletion, limit total dose, avoid concomitant therapy, PK monitoring, once daily dosing

Describe the treatment of aminoglycoside nephrotoxicity

discontinue the agent and other nephrotoxic drugs if possible, maintain hydration, supportive case Typically reversible, although short term renal replacement may be necessary

What is the incidence of radiographic contrast-media-induced nephrotoxicity

10 to 13%

describe the presentation of radiographic contrast-media-induced nephrotoxicity

presents within first 24 to 48 hours after admission serum creatinine peaks between three and four days after exposure recovery after 7 to 10 days irreversible AKI has been reported

Describe the mechanism of radiographic contrast-media-induced nephrotoxicity

Renal Ischemia (systemic hypotension and acute vasoconstriction) Direct cellular toxicity

Describe the risk factors for radiographic contrast-media-induced nephrotoxicity

Pre-existing kidney disease (most important) Decreased renal flow (CHF, volume depletion, hypotension) Diabetes Concurrent use of nephrotoxins

Describe the prevention of radiographic contrast-media-induced nephrotoxicity

Assess patient for risk factors Use alternative imaging in high-risk patient (ultrasound, MRI) Contrast: use noniodinated contrast, minimize contrast volume/dose, use low contrast agents Avoid nephrotoxic drugs Hydration: Isotonic saline infusion (3 to 12 hours prior and continue 6-24 hours after exposure) at rate of 1-1.5 mL/kg/hr to maintain urine rate of 150 mL/hr Urgent cases: 0.9%NaCl at 3mL/kg/hr beginning at 1 hour prior and continue for 6 hours after

How should you manage hydration in the prevention of radiographic contrast-media-induced nephrotoxicity

Isotonic saline infusion (3 to 12 hours prior and continue 6-24 hours after exposure) at rate of 1-1.5 mL/kg/hr to maintain urine rate of 150 mL/hr Urgent cases: 0.9%NaCl at 3mL/kg/hr beginning at 1 hour prior and continue for 6 hours after

Describe the treatment of radiographic contrast-media-induced nephrotoxicity

no specific therapy supportive care: discontinue other nephrotoxic drugs, delay subsequent contrast studies

Describe the incidence of amphotericin B nephrotoxicity

Variable rates Dose-dependent

Describe the presentation of amphotericin B nephrotoxicity

Non-oliguria, rise in Scr and BUN Renal tubular potassium, sodium and magnesium wasting Distal renal tubular acidosis Onset: few days to weeks Tubular dysfunction 1-2 weeks after initiation

Describe the mechanism of amphotericin B nephrotoxicity

Direct tubular epithelial cell toxicity --Necrosis of proximal tubular cells Afferent arteriolar vasoconstriction --Reduction in renal blood GFR

What are some risk factors for amphotericin B nephrotoxicity

Pre-existing kidney disease Large individual and cumulative doses Short infusion time Volume depletion Hypokalemia Increased age Concomitant administrations of diuretics and nephrotoxin

Describe the prevention of amphotericin B nephrotoxicity

Liposomal formulation Limiting cumulative doses Increasing infusion time Avoiding other nephrotoxic meds Hydrating patient ---1L of 0.9% NaCl IV daily during therapy OR ---10 – 15 mL/kg prior to amphotericin B Use other antifungals

describe the treatment of amphotericin B nephrotoxicity

Discontinue therapy and substitute with alternative antifungal Tubular damage will improve gradually but may be irreversible in some patients Monitor Scr and BUN daily Monitor K, Mg and correct as needed

Describe the mechanism of toxicity of drug induced acute interstitial nephritis

Systemic manifestation of hypersensitivity reaction Caused by medications, infections or connective tissue disease

Describe the presentation of drug induced acute interstitial nephritis

Presents days to weeks (usually 14 days) after drug exposure Fever, rash, arthralgia, eosinophilia

Describe the risk factors for drug induced acute interstitial nephritis

there are none

describe the prevention for drug induced acute interstitial nephritis

you can't

is drug induced acute interstitial nephritis reversible

yes

what are some drugs that can cause drug induced acute interstitial nephritis

Penicillin Cephalosporin NSAIDs Diuretics PPI

Describe the treatment of drug induced acute interstitial nephritis

Discontinue offending medication If renal failure > 7 days, steroids (High dose prednisone 1mg/kg/day for 4 to 6 weeks with taper over 4 weeks can be considered)

Describe the dose of steroids that may be used if the patient develops renal failure from drug induced acute interstitial nephritis

High dose prednisone 1mg/kg/day for 4 to 6 weeks with taper over 4 weeks can be considered

Describe it the mechanism of toxicity for drug induced post renal acute renal failure

Obstruction of urine flow from crystal formation or retroperitoneal fibrosis

What are some risk factors for drug induced post renal acute renal failure

Severe volume depletion Underlying renal insufficiency Bolus drug administration Metabolic acidosis or alkalosis

What are some drugs that can cause drug induced postrenal acute renal failure

Acyclovir Sulfonamides Methotrexate High dose vitamin C Indinavir, atazanavir

Describe the prevention of drug induced post renal acute renal failure

urine alkalinization

describe the treatment of drug induced post renal acute renal failure

stop the offending agent, replace volume, alkalinize urine

How do you find total body water for males

.6 x weight

how do you find total body water for females

.5 x weight

how do you find the intracellular fluid volume

2/3 of total body water

how do you find the extracellular fluid volume

1/3 of total body water

how do you find the volume of water that is in the interstitial space

3/4 of extracellular fluid (extracellular fluid is 1/3 of body water)

how do you find the volume of plasma

1/4 of extracellular fluid (extracellular fluid is 1/3 of body water)

What is the major determinant of water loss

ADH (Vasopressin)

what is another name for ADH

Vasopressin

what is another name for Vasopressin

ADH (anti diuretic hormone)

how does ADH act at low levels

increases water reabsorption

how does the ADH act at high levels

leads to vasoconstriction and increases in blood pressure

What are some signs and symptoms of volume depletion

Thirst, dry mouth, skin turgor Tachycardia Hypotension Oliguria Can range from mild to severe

what are some signs and symptoms of volume overload

Weight gain Increased urine volume Peripheral edema Pulmonary edema Rales Distended neck vein

She described the tonicity of crystalloids

Isotonic Hypotonic Hypertonic

describe the tonicity of colloids

Hypertonic (ONLY)

what are some examples of crystalloids

NS 3% NS ½ NS D5W LR

what are some examples of colloids

Albumin (5% or 25%) Hetastarch Plasmanate Blood

Describe normal saline (what it contains, tonicity, and uses)

0.9% NaCl Isotonic solution ECF 100% distribution, used for intravascular fluid replacement (resuscitation, hypotension, septic shock, etc.) Sodium and/or chloride replacement

Describe half normal saline (what it contains, tonicity, and uses)

0.45% NaCL Hypotonic solution Used for MIVF, often in combination with D5W Some intracellular (ICF) distribution

Describe 3% NaCl (tonicity, and uses)

Hypertonic solution, often used to treat hyponatremia

Describe Lactated Ringers (what it contains, tonicity, and uses)

Used for replacement of blood/fluid loss, approximates human plasma ECF distribution, isotonic solution Used in resuscitation (i.e. burns, trauma, acute pancreatitis, etc.) Contains 4 mEq/L of potassium

Describe D5W(what it contains, tonicity, and uses)

Dextrose 5% in water Hypotonic solution Used for free water replacement if dehydrated or hypernatremia Mainly ICF distribution NOT a resuscitative fluid and NOT a MIVF by itself

Describe where NS goes, and what impact it has on free water

100% goes into ECF and it adds no free water

Describe where half NS goes, and what impact it has on free water

2/3 goes into ECF, 1/3 goes into ICF. It adds 500 mL of free water per L

Describe where 3% NaCl goes, and what impact it has on free water

100% goes into ECF and it causes a loss of 2331 ml per L

Describe where LR goes, and what impact it has on free water

97% goes into ECF, 3% into ICF, no impact on free water

Describe where D5W goes, and what impact it has on free water

1/3 into ECF, 2/3 into ICF. Adds 1 L of free water per L

When do you use maintenance in fluid therapy, and what method is preferred

meet daily water requirements Indicated in patient unable to tolerate oral fluids Given as continuous infusion Crystalloid solutions preferred

When do you use Replacement/resuscitation in fluid therapy, and what method is preferred

restore intravascular volume and prevent organ hypo-perfusion Crystalloid or Colloid solutions Crystalloid solutions preferred (LR or NS) ---Inexpensive --- Readily available --- Less ADRs --- Provides electrolyte replacement

How do you estimate daily fluid requirements

30 – 40 mL/kg/day

What is the equation to calculate osmolality, and how accurate is it

Osm = (2 x Na) + (BUN/2.8) + (Glucose/18) Should predict measured within 5-10 mOsm/kg

How do you know if there is an osmolality gap and what does it mean

Osmolality Gap (OG) exists if difference b/w measured and calculated is > 15 OG = presences of unidentified particles

What is the normal serum sodium range

Normal serum range: 135-145 mEq/L

One is hypertonic hyponatremia most frequently seen

in elevated blood glucose

What are these severe symptoms of hypovolemic hyponatremia

altered mental status, seizures Metabolic encephalopathy can develop: ---Cerebral edema, Increased intracranial pressure (ICP), Irreversible and fatal

How do you treat symptomatic hypovolemic hyponatremia

May need to treat with 3% NaCL at a rate of 1 – 2 mEq/L until symptoms resolve Reasonable short-term goal = 120 mEq/L, Complete correction is unnecessary Calculate sodium replacement, give ½ the deficit over the first 8 hours, recheck Na, then ½ over the next 16 hrs

What can happen if you correct sodium deficiency too fast

If corrected too rapidly -> diffuse demyelinating lesions (central pontine myelinolysis)

How do you replace sodium

Give ½ the deficit over the first 8 hours, then ½ over the next 16 hrs May use 0.9% NaCl if asymptomatic, 3% NaCl is symptomatic

Define hypotonic hyponatremia

osmolality <275, Na <135 mEq/L

Define pseudo hyponatremia

Osm 275-290, , Na <135 mEq/L

Define hypertonic hyponatremia

Osm >290, , Na <135 mEq/L

Define hypovolemic hypotonic hyponatremia

decrease in total body water, osmolality <275, Na <135 mEq/L

define isovolumic hypotonic hyponatremia

no change in total body water, osmolality <275, Na <135 mEq/L

define hypervolemic hypotonic hyponatremia

increase in total body water, osmolality <275, Na <135 mEq/L

When dealing with hypertonic hyponatremia what should you adjust the sodium based on

adjust sodium based on blood glucose

If a patient has pseudohyponatremia what is the most likely cause

elevated triglycerides/protein

What is the first step in treating hypernatremia

calculating the free water deficit

what solutions can be used to fix free water deficit

Use hypotonic solution: D5W or 0.45% NaCl

How quickly should you replete volume in hypernatremia

Give ½ of total deficit over 24 hrs Give remaining ½ over the next 24-48 hrs as needed Goal is 0.5 mEq/L/hr decrease in Naserum (max of 12 mEq/L/day)

How often should you monitor serum Na in hypernatremia

Check q 8 hrs over the first 24 hrs

What is the normal range of potassium

3.5 – 5 mEq/L

what is the primary intracellular cation

Potassium

describe potassium's role in the body

Responsible for cell metabolism, glycogen and protein synthesis Determines the resting potential across cell membranes in cardiac and non-cardiac tissue Hypo and hyperkalemia associated with potentially fatal cardiac arrhythmias

what are some factors that affect potassium

Na/K ATPase pump, Kidneys, Arterial pH/acid-base status Medications: ACEI, ARB, Aldosterone antagonist, loop diuretics, HCTZ

How do you treat hypokalemia

Increase in potassium rich foods 10 mEq of IV or PO potassium will increase serum potassium by 0.1 mEq/L Chronic treatment with thiazide/loop diuretics may require KCl replacement 20 mEq per day orally is typical prophylactic dose

What is an important note when dosing PO potassium

Limit single PO dose to 60 mEq to avoid GI discomfort/irritation

describe monitoring during acute replacement of potassium

Acute replacement – monitor daily inpatient

describe monitoring during chronic replacement of potassium

Chronic replacement – varies, monitor weekly or monthly

When should IV potassium be used

Severe cases of hypokalemia Exhibiting signs of symptoms: EKG changes, muscle spasm

what are some precautions when using IV potassium

thrombophlebitis and pain at infusion, higher risk of leading to hyperkalemia

how do you administer IV potassium

Administration: Generally 10 – 20 mEq is diluted in 100 mL NS or D5W ---Infusion rate without cardiac monitoring -> 10mEq/hr ---With continuous cardiac monitoring -> 20 mEq/hr

Describe the five steps in treating hyperkalemia

Step 1 – Stop administration of all potassium sources Step 2 – Obtain EKG, if significant changes then: ----Administer 1gm of calcium gluconate intravenously ----Will work within 5 minutes and last for 30 minutes Step 3 – Shift potassium intracellularly ---Regular insulin (10 units) IV +/- D50W (dextrose 25 gm) give if BG is WNL ---Albuterol 10-20mg inhalation ---Sodium Bicarbonate 50 – 100 mEq IV if acidotic Step 4 – Remove potassium from body ---Diuresis, Dialysis, Potassium binders Step 5 – Identify and manage underlying causes of hyperkalemia

Describe the mechanism of action of calcium gluconate when used in hyperkalemia

Raises cardiac threshold potential

Describe the mechanism of action of regular insulin when used in hyperkalemia

Stimulates intracellular K uptake

Describe the mechanism of action of D50W when used in hyperkalemia

Stimulates insulin release, intracellular K uptake, given with regular insulin

Describe the mechanism of action of sodium carbonate when used in hyperkalemia

Raises serum pH, stimulates intracellular K uptake

Describe the mechanism of action of albuterol when used in hyperkalemia

Stimulates intracellular K uptake

Describe the mechanism of action of furosemide when used in hyperkalemia

Inhibits renal Na reabsorption, removes K from the body

Describe the mechanism of action hemodialysis when used in hyperkalemia

Removal of plasma and K

Describe the mechanism of action of Sodium polystyrene sulfonate (Kayexalate®) when used in hyperkalemia

Resin exchanges Na for K in intestine, excreted via feces

Describe the mechanism of action of Patiromer (Veltassa®) when used in hyperkalemia

Cation ion exchange polymer, potassium binder, increases fecal potassium excretion

Describe the mechanism of action of Sodium zirconium cyclosilicate (Lokelma®)when used in hyperkalemia

Potassium binder, exchanges K for Hydrogen and sodium, excreted via feces

What drugs can be used in the chronic treatment of hyperkalemia

Sodium polystyrene sulfonate Patiromer Sodium zirconium cyclosilicate

What are some important counseling points when using Sodium polystyrene sulfonate

Use limited by questionable efficacy, lots of drug interactions, ADEs Longer duration to work Take with food, must be refrigerated Administer other oral medication at least 3 hours before or 3 hours after

what are some important counseling points when using Patiromer

Effective for management of hyperkalemia, not for emergency management ADEs are known and seem minimal primarily GI and hypomagnesemia Must be refrigerated, stable for 3 months at room temperature Low risk of drug-drug interactions with other oral medications Administer other oral medication at least 3 hours before or 3 hours after

What are some important counseling points when using Sodium zirconium cyclosilicate

Approved May 2018 for hyperkalemia, not approved for emergency management No long term studies Mild ADE, GI and mild edema with higher doses Administer other oral medication at least 2 hours before or 2 hours after

What are some PO treatment options for hypomagnesemia and when do you use them

For asymptomatic patients Mag Oxide 400 – 800 mg

what are some IV treatment options for hypomagnesemia and when do you use them

Symptomatic patients (or cannot tolerate PO) Mg 1 – 4 gm IV once; Infuse 1 gm per hour

describe the treatment of hypomagnesemia

replace magnesium correct concomitant electrolytes such as potassium identify and correct underlying cause

Describe the treatment of hypermagnesemia

Reduce magnesium intake Calcium chloride 1 -2 gm IV x 1 and repeat prn (for cardiac complications) If adequate renal function: ---IV hydration with NS or 1/2NS at ~150 ml/hr + 1 – 2 grams of Ca ---IV furosemide to eliminate Mg If renal dysfunction ---Hemodialysis Supportive care (as needed) ---Cardiac pacing ---Vasopressors ---Mechanical ventilation

What buffer systems do we have in our body and how quickly do they act

Extracellular/intracellular – immediately action Respiratory regulation –fast onset (minutes) Renal regulation – slower onset

Which blood is used to determine blood gas

Arterial blood gases are our best source for obtaining these values, venous blood gases are easier to obtain

A pH below what is considered acidemia

7.35

a pH above what is considered alkalemia

7.45

How do you determine the primary process of acidosis or alkalosis

see if pCO2 or HCO3 is out of range

What values show metabolic acidosis or alkalosis

HCO3 < 24: Metabolic Acidosis HCO3 > 24: Metabolic Alkalosis

What values indicate respiratory acidosis or alkalosis

PCO2 < 40: Respiratory Alkalosis PCO2 > 40: Respiratory Acidosis

How do you interpret winter's formula

winter's formula gives you the calculated pCO2 If pCO2 is within the range that winters formula gives, the respiratory system is responding appropriately If pCO2 is higher than calculated, a respiratory acidosis is present If the pCO2 is lower than calculated, a respiratory alkalosis is present

How do you interpret the and nylon gap value

Normal Anion Gap (AG) ~12 If AG > 12: indicates an Anion Gap Metabolic Acidosis (AGMA) If AG ≤ 12: normal anion gap metabolic acidosis (NAGMA)

when do you calculate the delta gap and how do you interpret it

calculate the delta gap one the anion gap is greater than 12 Between -6 and 6: only AGMA If < -6: combined AGMA and normal anion gap metabolic acidosis (NAGMA) If > 6: combined AGMA and metabolic alkalosis

What are some causes of anion gap metabolic acidosis

hint - A CAT MUDPILES A – Analgesics (massive NSAIDS, acetaminophen) C – Cyanide, Carbon monoxide A – Arsenic, Alcoholic ketoacidosis T - Toluene M – Methanol, Metformin U - Uremia D – Diabetic ketoacidosis P – Paraldehyde, Phenformin I – Iron, Isoniazid L – Lactic acidosis E – Ethylene glycol S – Salicylates

What are some causes of lactic acidosis

Shock (decreased tissue oxygenation) Drugs/toxins --Ethanol --Metformin --Nucleoside Reverse Transcriptase Inhibitors (NRTIs) --Propylene Glycol Toxicity --Propofol Infusion Syndrome --Sodium nitroprusside

What is another name for non-anion gap acidosis

hyperchloremic acidosis

Describe the pathophysiology of non-anion gap acidosis

Loss of plasma HCO3- replaced by Cl-, thus AG remains normal

What are some causes of decreased carbonic acid that can lead to non-anion gap acidosis

GI tract waste --Diarrhea --Pancreatic fistulas/biliary drainage Renal loss of HCO3- --Proximal Renal tubular acidosis Impaired renal acid excretion --Distal renal tubular acidosis

describe some causes of proximal renal tubular acidosis (type 2)

Toxins (Pb, Cd, Hg, or outdated tetracyclines) Carbonic anhydrase inhibitors (acetazolamide)

Describe some causes of distal renal tubular acidosis, type one (hypokalemia)

amphotericin B, lithium, toluene, vitamin D intoxication

Describe some causes of distal renal tubular acidosis, type 4 (hyperkalemia)

Causes: ACEI, ARBs, Spironolactone

What are some causes of metabolic alkalosis

Increase HCO3- --Infusion of acetate, lactate, or citrate --Administration of HCO3- Excessive H+ losses --GI loss of H+ via vomiting/NG suctioning --Renal loss of H+

What are the ABCDs of drug overdose

Airway Breathing Circulation drug induced CNS depression

What are some airway signs and symptoms to be evaluating when a poisoned patient comes in, and what would be a reasonable treatment if you see such signs and symptoms (initial management)

Symptoms – dyspnea, dysphonia, air hunger, hoarseness Signs – stridor, retractions, cyanosis

What are some treatments for airway signs and symptoms

Treatment – Intubation

What are some breathing makers that should be evaluated when a poisoned patient comes in, and what would be a reasonable treatment if you see such signs and symptoms (initial management)

Oxygenation – pulse oximetry Treatment – 100% O2 via facemask (except in those with elevated pCO2 levels)

What are some circulation makers that should be evaluated when a poisoned patient comes in, and what would be a reasonable treatment if you see such signs and symptoms (initial management)

Pulse Blood pressure Treatment – need a line placed, give a fluid bolus

What is the coma cocktail, and when is it used

Dextrose – give 50mL of 50% dextrose IV Thiamine – 100mg IV Naloxone – 0.4-2.0mg in most, lower doses in suspected opioid addiction Usedin treatment of drug induced CNS depression

Why would you give thiamine

for alcohol poisoning

What questions should you be asking when looking at history of an exposure

Description of exposure (events and symptoms that occurred) Co-ingestions? Any therapy/first aid given? Agents involved (physical evidence?) Routes of administration Amount administered Time since exposure

What are some questions you should be asking when evaluating medical history

Allergies Medications Past medical history Situation prior to event Height and weight

What should you be evaluating in the physical exam

LOOK at the PATIENT LOOK at the SKIN SMELL patient's BREATH LISTEN to the LUNGS LISTEN to the HEART EXAMINE ABDOMEN EXTREMITIES/NEURO EXAM

What labs may you do for patients who have come in for an overdose

Metabolic profile/Chemistries Electrolytes CBC Anion gap Osmolal gap Serum tox screen Urine tox screen (may give false +/-) Quantitative analysis

What is the definition of toxicokinetics

Toxicokinetics is the absorption, distribution, metabolism, and excretion of drugs at doses associated with clinical toxicity

Which aspects of ADME may be affected in an overdose

all

What are some ways that our body systems may change in an overdose that could affect ADME

GI motility (increased or decreased) Cardiovascular/Pulmonary Function (overworking or underworking) Acid-Base disturbances (ion trapping) Kidney/Liver function (reduced ability to eliminate drugs) Hypothermia (changes blood flow)