Point of Care Chem8 Use in the Urgent Care Setting - PowerPoint Presentation

Slide1

Point of Care Chem8 Use in the Urgent Care Setting

Minal Desai, MDJake Lagomarcino, PAStephanie LiVecchi, PABetty Masten, MDMeagan Puckett, FNP

Click to add text

Slide2

POC CHEM8

POC BMP Includes: Ionized CalciumPotassiumSodiumGlucose

BUN

Creatinine

CO2Anion Gap

Cost for POC BMP Testing:$60.58Self Pay: $16.94

CPT CODE for Ordering is 80048

Slide3

Diabetic Ketoacidosis (DKA)

Ketoacidosis and hyperglycemiaOccurs rapidly, usually over 24 hoursHyperosmolar Hyperglycemic State (HHS)More severe hyperglycemiaNo ketoacidosisSlower onset

Slide4

Clinical Manifestation DKA

Polyuria, polydipsia, weight lossAbdominal symptomsNausea, vomiting, abdominal painNeurological symptomsMore common in HHS (coma, obtundation, seizures)

Diagnostic Criteria

Hyperglycemia (usually <800)

Anion gap metabolic acidosis

Ketonemia

Slide5

Diagnostics

Serum glucoseSerum electrolytes (with anion gap)BUNPlasma creatinineCBC w/ differentialUA and urine ketones by dipstickPlasma osmolalitySerum ketones (if urine ketones are present)ABCEKG

Findings in DKA

Hyperglycemia

Hyponatremia

K+ usually normal, about 1/3 of patients have hyperkalemia

Elevated BUN

Elevated plasma creatinine

Slide6

DKA

In urgent care, if we suspect DKA, likely the patient will be going to the Emergency Department

We may however, considering using the BMP to rule out DKA in a patient that we have low suspicion to begin with

Slide7

Management of abnormal anion gap levels

DKA usually presents with a serum anion gap greater than 20 mEq/LSerum anion gap = serum sodium - (serum chloride + bicarbonate)

Slide8

Management of abnormal Glucose levels

K+ is the key electrolyte to pay attention toInitiate treatment with low-dose IV insulin in all patients with moderate to severe DKA or HHS who have a serum potassium ≥3.3 mEq/LIf serum potassium is <3.3mEq/L, insulin will worsen hypokalemia by driving potassium into the cellsTherefore, be aggressive with fluid and potassium replacement prior to treatment with insulin

Slide9

Management of abnormal glucose levels

HypoglycemiaHyperglycemia

Slide10

Hyperglycemia

DefinitionHyperglycemiaNon-Fasting > 140Fasting > 120Diabetes:

Symptomatic and Random BG > 200

 

Asymptomatic and FBG > 120PrediabetesFasting Blood Glucose 100-120

Slide11

Hyperglycemia

Clinical PresentationAsymptomatic-Common in  Type II diabetes, PrediabetesSymptomatic-more common in Type I diabetesPolyuria

Polydipsia

Weightloss

See DKA

Slide12

Hyperglycemia

CausesDiabetes Type II Most common in adults, older onset, often asymptomatic or milder symptomsDiabetes Type I-Suspect in younger patients (even if obese), lean body mass, no signs of metabolic syndrome, Catabolic state (weight loss and ketones), BS >300

Pre

diabetes

Stress HyperglycemiaGlucocorticoids

Slide13

Hyperglycemia

Management-known DiabeticRule out DKA or Hyperosmolar hyperglycemia(see previous slides)Evaluate for concurrent illnessReview Diabetes treatment plan

Arrange close follow up with PCP or Endocrine

Slide14

Hyperglycemia

Management-New Onset DKA-to ED (see previous slides) 30% of new onset in pediatric patientsHyperglycemia with signs of catabolic state: Needs prompt evaluation by Endocrine. Most often will need ED for further evaluation

Asymptomatic or very mild symptoms:

Prompt follow up with PCP or Endocrine

Slide15

Hypoglycemia

Definition- Treated DiabetesADA  definition: abnormally low BG concentration  that expose the individual to harm. Varies in individualsAlert Level: Blood Sugar < 70 mg/dL

Severe Biochemical Hypoglycemia:

BS < 54

Slide16

Hypoglycemia

Definition-NonDiabetes-Whipple Criteria Plasma glucose concentration low enough to cause signs and symptoms of brain dysfunction (neuroglycopenia)Blood Sugar < 50 mg/dLResolution of symptoms with treatment 

Slide17

Hypoglycemia

Clinical ManifestationsNeurogenic(autonomic)*-BS 55-60 SweatingTremorsPalpitationsTachycardiaHunger*Individual variations. Sometimes response blunted by

repeated episodes

Slide18

Hypoglycemia

Clinical ManifestationsNeuroglycopenic(CNS)-BS < 50LethargyConfusionIrritabilityLoss of ConsciousnessSeizures

Slide19

Hypoglycemia

Clinical ManifestationsInfants and Toddlers-non-specificJitteryTremorIrritabilityPoor feedingLethargyCyanosis

Seizures(Often first symptoms)

Slide20

Hypoglycemia

CausesTreated Diabetes!!!Ingestion: accidental or maliciousDrug ReactionETOHCritical Illness

Less Common: metabolic disorders, Insulinoma,

functional hyperinsulinemia including after Gastric Bypass surgery

Slide21

Hypoglycemia

managementAsymptomaticAvoid critical tasks (driving)Ingest carbohydratesRepeat measurementsAdjust treatment regimen

Slide22

Hypoglycemia

managementSymptomatic15-20 gms Fast Acting CarbohydratesRetest 15 minutesRepeat Fast acting carbohydrates as neededLong-acting Carbohydrates (eat a meal)Adjust treatment regimen

Slide23

Hypoglycemia

managementSevere-with CNS symptomsGlucagon or IV Dextrose  (but do not delay Glucagon if no IV access)Glucagon not effective if non-insulin mediated disease process. This can be a diagnostic tool for other causes such as insulinoma or metabolic disease

IV access with continuous Glucose solution 

Transport to ED

Slide24

Hypercalcemia Symptoms

"Stones" refers to kidney stones

, 

nephrocalcinosis

, and diabetes insipidus

 (polyuria and polydipsia). These can ultimately lead to kidney failure."

Bones"

refers to bone-related complications. The classic bone disease in hyperparathyroidism is 

osteitis fibrosa cystica

, which results in pain and sometimes pathological fractures. Other bone diseases associated with hyperparathyroidism are 

osteoporosis

, 

osteomalacia

, and 

arthritis

.

"

Abdominal groans

" refers to gastrointestinal symptoms of 

constipation

, 

indigestion

, 

nausea

 and 

vomiting

. Hypercalcemia can lead to 

peptic ulcers

 and 

acute pancreatitis

. The peptic ulcers can be an effect of increased 

gastric acid

 secretion by hypercalcemia.

[1]

"Thrones"

refers to polyuria and constipation

"

Psychiatric overtones

" refers to effects on the 

central nervous system

. Symptoms include lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and coma.

Slide25

APPROACH TO eLEVATED cA++

90% of Hypercalcemia is from Hyperparathyroidism or cancerHypercalcemia may be associated with a spectrum of clinical manifestations, ranging from few or no symptoms in patients with mild chronic hypercalcemia to severe obtundation and coma. The degree of hypercalcemia, along with the rate of rise of serum calcium concentration, often determines symptoms and the urgency of therapy. The therapeutic approach should reflect these differences 

Mild to moderate hypercalcemia with mild

sx

(I.e. constipation) can be managed outpatient in most scenarios

Severe rises (usually patient with present with stupor or similar should go to ER for aggressive management (fluids and various meds) 

Slide26

Hypocalcemia Symptoms

The hallmark of acute hypocalcemia is tetany, which is characterized by neuromuscular irritability. The symptoms of tetany may be mild (perioral numbness, paresthesias of the hands and feet, muscle cramps) or severe (carpopedal spasm, laryngospasm, and focal or generalized seizures

Tetany is uncommon unless the serum ionized calcium concentration

falls below 4.3 mg/dL

Cardiac

*Prolonged QT

Heart Failure

Arrythmia (less common than K or Mg)

Psych manifestations- anxiety depression, rarer would be confusion

Slide27

Hypocalcemia

Diseases:Hypoparathyroidism (need life-long vit D and calcium supplementation)Vit D deficiency Chronic Kidney Disease

Chronic Liver Disease

Autosomal dominant hypocalcemia (ADH) (rare)

Pseudohypoparathyroidism (

group of heterogeneous disorders defined by target organ (kidney and, perhaps, bone) unresponsiveness to PTH) 

Slide28

Inhibitors

of bone resorption (bisphosphonates, calcitonin, denosumab)Calcium chelators (EDTA, citrate, phosphate)FoscarnetCinacalcet

Meds Causing Low Ca

Diuretics

Lithium

Synthetic parathyroid hormone drugs

Meds Causing High Ca

Slide29

Hypocalcemia Treatment

Symptoms

(eg, carpopedal spasm, tetany, seizures)

A prolonged QT interval

In asymptomatic patients with an acute decrease in serum corrected calcium to ≤7.5 mg/dL (≤1.9 mmol/L) or

ionized calcium to ≤3 mg/dL

(≤0.8 mmol/L), who may develop serious complications if untreated. Acute hypocalcemia can occur when there is a rapid and progressive reduction in serum calcium (eg, acute hypoparathyroidism following post-radical neck dissection for head and neck cancer).

For those with milder symptoms of neuromuscular irritability (paresthesias) and a serum ionized calcium concentration

greater than 3.0 mg/dL

(0.8 mmol/L), initial treatment with

oral

calcium supplementation is sufficient 

Slide30

 mmol/L  1.15 – 1.33

mg/dL  4.6 – 5.3 mEq/L  2.3 – 2.7Ca++ Reference Ranges

Slide31

A message from Dr. Fink

The total serum calcium concentration consists of three fractions (see 'Determinants of the serum calcium concentration' above):•15 percent is bound to organic and inorganic anions

•40 percent is bound to albumin

•45 percent is physiologically active ionized (or free) calcium

●Measurement of the total serum calcium concentration alone is often misleading; thus, measurement of ionized calcium remains the gold standard for assessing calcium status. Clinical scenarios in which total calcium can change without affecting the concentration of ionized calcium include:

•Hypoalbuminemia because a large fraction of calcium circulates while bound to albumin.

•Hyperalbuminemia, as may occur with extracellular volume depletion or by fluid movement out of the vascular space due to a tight tourniquet, and can also result from a very high-protein diet.

•Some cases of multiple myeloma, in which calcium binds to the monoclonal immunoglobulin. (See 'Multiple myeloma' above.)

●The ionized fraction can change without an alteration in the total serum calcium concentration, as with:

•Acid-base disorders, in which an increase in blood pH may enhance binding of calcium to albumin, thereby decreasing the ionized fraction. (See 'Acid-base disorders' above.)

•Hyperparathyroidism, which increases the ionized calcium at the expense of that bound to albumin. (See 'Parathyroid hormone' above.)

•Hyperphosphatemia, which increases the fraction bound to inorganic anions, decreasing ionized calcium. (See 'Hyperphosphatemia' above.)

Slide32

Hypertension

Blood pressure and kidney disease has special relation as high blood pressure can damage kidneys and flip is true as several kidney diseases can cause high BP. Hypertension causes excess pressure on blood vessels which starts scarring of blood vessels and damage kidneys . On the other hand abnormal /excess stimulation of renin sympathomimetic system due to several triggers can lead to high BP.HTN induced kidney damage can be acute ( <3 months ) -AKI or it can be chronic ( > 3 months ) - CKD.

Slide33

Hypertension/Medication Management

Pts with HTN with or without CKD needs wise choice of medication to control HTN . Some of the common side effects of antihypertensives -Diuretics-  electrolyte abnormalities including hypokalemia, hypercalcemia , increases BSL in DM . ACEI- can worsens pre-existing AKI or damage kidneys faster in patient on nephrotoxic medications. 

BMP beforehand can help to decide best choice of antihypertensive .

Slide34

Hypertension/Medication Management

Hence BMP result avaliability in clinic can guide provider in several ways.Diuretic as first choice in person with no other medical conditions if BMP is normal. ACEI or ARBs in patient with DM , CKD where bmp is abnormal. BB and ACEI / ARB in patient with  CAD with abnormal BMP.

Slide35

Acute Kidney Injury

Acute kidney injury is a clinical syndrome characterized by a rapid decline in glomerular filtration rate and resultant accumulation of metabolic waste products. Acute kidney injury is associated with an increased risk of mortality, cardiovascular events, and progression to chronic kidney disease. Severity of acute kidney injury is classified according to urine output and elevations in creatinine level. Etiologies of acute kidney injury are categorized as prerenal, intrinsic renal, and postrenal. Accurate diagnosis of the underlying cause is key to successful management

Slide36

STAGE

CHANGE IN SERUM CREATININE LEVEL

URINE OUTPUT

OTHER

1

Increase ≥ 0.3 mg per dL (26.52

μ

mol per L) or ≥ 1.5- to twofold from baseline

< 0.5 mL per kg per hour for more than six hours

—

2

Increase > two- to threefold from baseline

< 0.5 mL per kg per hour for more than 12 hours

—

3

Increase > threefold from baseline or ≥ 4.0 mg per dL (353.60

μ

mol per L) with an acute rise of at least 0.5 mg per dL (44.20

μ

mol per L)

< 0.3 mL per kg per hour for 24 hours or anuria for 12 hours

Renal replacement therapy requir

Slide37

Acute Kidney Injury

The definition of acute kidney injury indicates that a rise in creatinine has occurred within 48 hours, although in the outpatient setting, it may be hard to ascertain when the rise actually happened. A high serum creatinine level in a patient with a previously normal documented level suggests an acute process, whereas a rise over weeks to months represents a subacute or chronic process.

Slide38

Increased creatinine secretion

 — Even with an accurate urine collection, the accuracy of the creatinine clearance as a measurement of GFR is limited by the fact that, at a normal GFR, 10 to 20 percent of creatinine excretion is derived from secretion in the proximal tubule, resulting in the creatinine clearance being 10 to 20 percent higher than the GFR. As the GFR falls, the associated reductions in creatinine filtration and excretion will result in an increase in serum creatinine, which provides the signal for enhanced creatinine secretion. The increase in secretion counterbalances the reduction in creatinine filtration so that a steady state is reestablished in which creatinine excretion is maintained at the same level as creatinine production with a slightly higher creatinine concentration than before [

2,4,9-11

]. However, the increase in creatinine secretion will result in the creatinine clearance being a progressively greater overestimate of the GFR.

As an example, as the true GFR falls from 80 to 40 mL/min (as measured by the clearance of an accurate filtration marker such as inulin or radioisotopic

iothalamate or DTPA) [10,12], the absolute amount of secreted creatinine can rise by more than 50 percent, accounting for as much as 35 percent of urinary creatinine [2

]. In this setting, creatinine excretion is much greater than creatinine filtration. As a result, calculation of the creatinine clearance from a 24-hour urine collection will represent a large overestimate of the true GFR. The net effect is that the creatinine clearance may be normal (>90 mL/min) in approximately one-half of patients with a true GFR of 61 to 70 mL/min and one-quarter of those with a true GFR of 51 to 60 mL/min [

9

]. Some patients with advanced disease have a creatinine clearance that exceeds the GFR by more than twofold."

Slide39

TYPE OF RENAL FAILURE

BUN-TO-CREATININE RATIO

URINE OSMOLALITY

FRACTIONAL EXCRETIONOF SODIUM*

Prerenal acute renal failure

> 20:1> 500

mOsm

< 1%

Intrinsic acute renal failure

< 20:1

250 to 300

mOsm

> 3%

 

Although the blood urea nitrogen (BUN) also varies inversely with the GFR, it is generally less useful than the serum creatinine because the BUN can change independently of the GFR. Two factors contribute to this phenomenon 

●

The rate of urea production is not constant, increasing with a high-protein diet and with enhanced tissue breakdown due to hemorrhage, trauma, or glucocorticoid therapy. By comparison, a low-protein diet or liver disease can lower the BUN without change in GFR. Thus, liver disease may be associated with near-normal values for both the BUN (due to decreased urea production) and the serum creatinine (due to muscle wasting) despite a relatively large reduction in GFR 

●

Approximately 40 to 50 percent of the filtered urea is passively reabsorbed, mostly in the proximal tubule. Thus, when volume depletion is associated with enhanced proximal sodium and water reabsorption, there is a parallel increase in urea reabsorption. As a result, the BUN will rise out of proportion to any change in GFR, and therefore to any change in the serum creatinine (

SCr

). This elevation in the BUN-to-

SCr

ratio is one of the suggestive clinical signs of decreased renal perfusion (prerenal disease) as the cause for renal failure. 

BUN

Slide40

Causes

***Remember we're only taking a snapshot

70%

of AKI are prerenal and underlying kidney function is normal

Pre-Renal:VasoconstrictionSepsis or vasodilation (shock)

Volume depletion (dehydration, DKA, etc)

Slide41

Intrinsic Renal

Tubular

Ischemia (prolonged hypotension

Toxins

Exogenous- poisonsEndogenous- Rhabdo

Interstitial:MedicationsInfections

Systemic disease (lupus, sarcoidosis

Vascular

Malignant HTN, Scleroderma renal crisis, thrombus (arterial or venous)

CHECK IT OUT!

AAFP-AKI

Table 3.

History and Physical Examination Findings for Categorizing Acute Kidney Injury

Slide42

Acute Kidney Injury

Slide43

AKI

Summary:Patients with acute kidney injury generally should be hospitalized unless the condition is mild and clearly resulting from an easily reversible cause. The key to management is assuring adequate renal perfusion by achieving and maintaining hemodynamic stability and avoiding hypovolemia.

Those

at highest risk include adults older than 75 years; persons with diabetes or preexisting chronic kidney disease; persons with medical problems such as cardiac failure, liver failure, or sepsis; and those who are exposed to contrast agents or who are undergoing cardiac surgery

Patients

with acute kidney injury are more likely to develop chronic kidney disease in the future. They are also at higher risk of end-stage renal disease and premature death

Slide44

Rhabdomyolysis

Rhabdomyolysis is muscle necrosis and release of intracellular constituents in the circulation.Volume depletion leads to renal ischemiaTubular obstruction due to heme pigment castsTubular injury from free iron.

CK has a longer

half-life

than myoglobin

Slide45

Clinical manifestations Rhabdomyolysis

Classic triad; muscle pain, fatigue, dark urineAdditional symptoms that are more common in severely affected patients include malaise, fever, tachycardia, nausea and vomiting, and abdominal painCommon to have metabolic acidosis

K                  Calcium           then you will get hypercalcemia as it will rapidly increase during recovery phase.

Risk of AKI is lower when CK is less than 20k

Slide46

Outpatient Treatment of Rhabdomyolysis

***Initial IV hydration, 1.5L per hour, maintain urine output, alkaline urine to a pH greater than 6.5Baseline CKFluids given regardless of renal functionUptodate recommends ECG as well

Elderly to ER, there is a total risk score you can use on 

uptodate

Alkalinization of the urine with intravenous sodium bicarbonate in select patients (normal calcium, bicarbonate less than 30 mEq per L [30 mmol per L], and arterial pH less than 7.5

Slide47

Management of abnormal BUN levels

Blood urea nitrogen produced in liver and is subsequently removed by kidneys. BUN varies inversely with the GFR but is less useful than creatinine because BUN can change independently of the GFR due to certain physiologic processes. BUN creatine ratio is more predictive of renal failure than BUN alone.High BUN level-  Heart failure, dehydration, high protein diet , nephrotoxic medications.Low BUN level- Liver disease, 2nd and 3rd trimester of pregnancy , steroids and antibiotics. Hence management of abnormal  BUN depends on management of underlying disease. 

Slide48

Hyperkalemia

A common problem.Potassium enters the body via oral intake or IV infusion, stored in the cells, excreted in the urine. Major causes: increased potassium release from the cells and reduced urinary potassium excretion (most common)Increasing potassium intake alone is not a common cause.Persistent hyperkalemia requires impaired urinary potassium excretion, associated with a reduction in aldosterone secretion or responsiveness, acute or chronic kidney disease, and/or diminished delivery of sodium and water to the distal potassium secretory sites. Potassium secretion is tightly regulated by a complex interplay among individual mediators in the renin-angiotensin-aldosterone system, sodium and potassium transport pathways, and the chloride-sensitive WNK signaling system. Due to aldosterone-independent regulatory pathways in potassium homeostasis, hyperkalemia is not a universal feature of

hypoaldosteronism

.

Slide49

Major Causes of Hyperkalemia

Increased potassium release from cells:Metabolic AcidosisInsulin deficiency, hyperglycemia, and hyperosmolality

Increased tissue catabolism

Beta blockers

Exercise Hyperkalemic periodic paralysis Other: Overdose of digitalis, Red cell transfusion, Succinylcholine, Activators of ATP-dependent potassium channels

Reduced Urinary Potassium Excretion:Reduced aldosterone secretion Reduced response to aldosterone Reduced distal sodium and water delivery Effective arterial blood volume depletion

Acute and chronic kidney disease

Other: Selective impairment in potassium secretion, Gordon's syndrome,

Ureterojejunostomy

Slide50

Clinical Manifestations Hyperkalemia

Typically occurs when serum Potassium is ≥ 7.0 mEq/L with chronic hyperkalemia, lower levels with acute rise.Muscle Weakness or ParalysisCardiac Conduction AbnormalitiesCardiac ArrhythmiasPolyuria and Polydipsia with uncontrolled diabetes

Slide51

ECG Changes with Hyperkalemia

Tall peaked T waves and Shortened QT interval = the First findingsLengthening of PR interval and QRS duration, P wave may disappear, and ultimately QRS widens to a sine wave pattern as hyperkalemia becomes more severe. Eventual ventricular standstill with flat line on ECG with complete absence of electrical activity.It is rare to have a normal ECG despite serum potassium > 9.0

mEq

/L

ECG abnormalities are more likely with rapid onset hyperkalemia and with the following other abnormalities: hypocalcemia, academia, and/or hyponatremia.ECG cannot be used to monitor efficacy of hyperkalemic therapy.

Type 1 Brugada Pattern on ECG with a pseudo-RBB and persistent ST elevation in at least 2 precordial leads. Occurs in critically ill patients with > 7.0 mEq/L potassium.Conduction Abnormalities: RBBB, LBBB,

Bifascicular

Block, Advanced AV Block.

Arrythmias

:

Sinus Bradycardia, Sinus Arrest, Slow IV Rhythms, Ventricular Tachycardia, Ventricular Fibrillation, Asystole.

Slide52

Reduced Urinary Acid Excretion

Hyperkalemia interferes with Renal Ammonium (NH4+) excretion, limiting acid excretion, leading to metabolic acidosis.3 Mechanisms thought to contribute to hyperkalemia-induced decrease in ammonia secretion:Intracellular Alkalosis as entry of excess potassium into cells is associated with hydrogen ion movement out of the cells. Reduces both ammonium excretion and bicarbonate reabsorption.

Reduced NH4+ reabsorption in thick ascending loop of Henle.

Diminished

ammoniagenesis, mediated partly by glutamate deamination.

Slide53

Treatment of Hyperkalemia

Hyperkalemic Emergency: ≥ 7.0 mEq/LRequires IV Calcium, IV Insulin, and IV GlucoseMay require Hemodialysis, GI Potassium Binders, or Diuretics

Severe Hyperkalemia

: ≥ 6.5

mEq/L (GI Bleeding even if no signs/sx)Moderate Hyperkalemia: > 5.5 mEq/L

Significant renal impairmentOngoing tissue breakdown: Rhabdomyolysis or crush injury, Tumor Lysis SyndromeOngoing Potassium absorption (substantial GI bleed)Significant non-anion gap metabolic acidosis or respiratory acidosisPrompt Therapy

: potassium lowered over 6-12 hours

HD patients, marginal renal function, marginal UOP, hyperkalemic patients pending surgery.

Isotonic Bicarb infusion, IV 5% Dextrose in water overnight (stimulates fast acting insulin), or HD.

May also receive potassium binders PO or

Kaliuresis

induced by IV saline w/ diuretic therapy.

Potassium Lowered Slowly

:

Chronic, mild ≤ 5.5 or Moderate 5.5-6.5

mEq

/L elevations due to CKD or medications that inhibit Renin-

Angiotension

-Aldosterone System or both.

Dietary modifications, use of diuretics (Loop or Thiazide), treatment of chronic metabolic acidosis, or reversal of causes (NSAIDs, Hypovolemia). May also d/c or reduce drugs that inhibit RAAS.

Slide54

Hypokalemia

Can be transiently induced by entry of potassium into the cells.Most commonly results from GI or urinary loss, i.e. vomiting, diarrhea, or diuretic therapy.Potassium replacement indicated when hypokalemia is due to potassium loss and significant deficit in the body. Also indicated for acute hypokalemia, thyrotoxic periodic paralysisPotassium replacement is given cautiously in redistributive hypokalemia due to rebound hyperkalemia potential.

Slide55

Clinical Manifestations of Hypokalemia

Symptoms do not typically manifest until Potassium is <3.0 mEq/L unless serum potassium falls suddenly: predisposition of arrhythmia due to Digitalis.Muscle Weakness Does not typically occur until potassium <2.5 mEq/L if slow developmentSignificant weakness at <2.5

Begins in LE, progresses to trunk and upper extremities. Can worsen to paralysis.

Muscle cramps,

Rhabdo, Myoglobinuria.

Respiratory muscle weakness, which can cause RF and death.Involvement of GI muscles leading to ileus, distention, anorexia, N/V.

Slide56

Clinical Manifestations of Hypokalemia

Cardiac Arrhythmias and ECG AbnormalitiesTypically occur with serum potassium ≤ 3.0PAC’s, premature ventricular beats, Sinus Bradycardia, Paroxysmal atrial or junctional tachycardia, AV block, Vtach, Vfib.

ST depression

Decreased amplitude of T wave

Increased amplitude of U waves (which occur at end of T wave).U waves are often seen in the lateral precordial leads V4-V6.

QT prolongation.Hypokalemia with associated Magnesium depletion (diuretics or diarrhea) both promote development of arrhythmias. Increased risk of Torsades de Pointes, esp in patients that take drugs that cause QT prolongation or genetic predisposition to QT prolongation.

Risk of Arrhythmia is highest in older patients, patients with organic heart disease, and patients on Digoxin or other antiarrhythmic drugs.

Slide57

Clinical Manifestations of Hypokalemia

Renal AbnormalitiesProlonged Hypokalemia causes structural and functional changes in the kidneysImpaired concentrationIncreased ammonia productionIncreased Bicarb reabsorption

Altered sodium reabsorption

Hypokalemic Nephropathy

Elevated BP.Glucose IntoleranceHypokalemia reduces insulin secretion, which may play a role in thiazide-associated diabetes.

Slide58

Treatment of LOW potassium

Goals: prevent life-threatening complications (arrhythmias, paralysis, rhabdo, diaphragmatic weakness), replace potassium deficit, diagnose and treat underlying causes.Many different Potassium preparations: Liquid is cheap but has poor taste. Preferred for feeding tubes or dysphagia.Slow release is better tolerated but has increased GI ulceration and bleeding risk.

IV potassium for patients who cannot take oral or as adjunct to oral therapy.

Potassium Rich food is less effective: bananas, oranges, molasses, seaweed, dried fruits, nuts, avocados, bran cereal, lima beans, spinach, tomatoes, potatoes, broccoli, cauliflower, etc.

Potassium Bicarb

: used w/ hypokalemia and metabolic acidosis (renal tubular acidosis or diarrhea)Potassium Chloride: PREFFERRED b/c hypokalemia and metabolic alkalosis often w/ chloride depletion (diuretics or vomiting).Raises serum potassium at a faster rate than potassium bicarb.

Slide59

Treatment of LOW potassium

Mild to Moderate Hypokalemia: (3.0-3.4 mEq/L): Typically treated with oral therapy, 10-20 mEq/L Potassium 2-4 times daily until K+ is persistently above 3.0-3.5.Severe of Symptomatic Hypokalemia: less than 2.5-3.0 mEq/L or symptomatic (arrhythmias, marked muscle weakness, rhabdo) typically need IV replacement.

Slide60

Dehydration/Heat stroke

Volume depletion results from loss of sodium and water through:GI loss: vomiting, diarrhea, bleedingRenal loss: diuretics, hypoaldosteronismSkin loss: sweat, burnsThird spacing: intestinal obstruction, crush injury, fracture, acute pancreatitisExertional heat stroke (what we will see more often)Usually young, otherwise healthy individuals who engage in heavy exercise during times of high temperatures and humidityNon-exertional heat stroke

Slide61

Dehydration/Heat stroke Presentation

Volume depletion: fatigue, thirst, muscle cramps, postural dizziness, decreased urinary volume/frequency. Abdominal pain, chest pain, lethargy, confusionFluid loss: vomiting, dirrhea, polyuria, severe skin burnElectrolyte abnormalities: Hypo or Hyperkalema > muscle weaknesHypokalemia > polyuria and polydipsiaAcidosis > tachypneaMetabolic alkalosis > neuromuscular irritability and confusionHypo or Hypernatremia > lethargy, confusion, seizures

elevated core body temperature, sinus tachycardia, tachypnea, a widened pulse pressure, and hypotension 

weakness, lethargy, nausea, or dizziness

Slide62

Dehydration/Heat stroke Diagnosis

UAUsually low urine volumeCMPBUN/creatinine usually elevatedSalt and water loss > hyponatremiaPrimary H2O loss or DI > hypernatremiaHypokalemia more commonAlkalosis > vomiting or diureticsAcidosis > diarrhea or intestinal fistulas lead to bicarb lossCBCHematocrit is typically elevated due to reduced plasma volumeAlbumin concentration typically elevated too

CBC & CMP

PT and PTT

Arterial or venous blood gasSerum CK and urine myoglobin (Rhabdo)Though, diagnosis is usually clinicalDiagnosis: elevated temperature, AMS, and exposure to severe heat

Slide63

HyperNatremia

Most often due to unreplaced H20 lost from GI tract (V/D), sweat, or urine (DI, Glycosuria, inc. urea excretion)Due to H20 loss = dehydration. Different from hypovolemia when both salt and H20 are lost.Common in ICU when patients are administered lg. amounts of fluids to correct hypovolemia or hypotension.

Severe symptoms usually require an elevation of serum Na- ≥158.

Values ≥ 180 associated with

HIGH mortality rate.

Acute: less than 48 hoursChronic: greater than 48 hours. Most common, even with acute symptoms.

Slide64

HyperNatremia: Clinical Manifestations

LethargyWeaknessIrritabilityTwitchingSeizuresComaRapid decrease in brain volume can cause rupture of cerebral veins  focal intracerebral and subarachnoid hemorrhages, possibly irreversible neurological damage.

Demyelinating brain lesions

Slide65

Management of Hypernatremia

Initial Fluid Replacement:A net positive balance of 3 mL of electrolyte-free H20 per kg will lower the serum sodium by approx. 1 mEq/LStep-wise approachCurrent TBW x (

Serum NA

-1 )

140Chronic Treatment:5% Dextrose in H2O IV at approx. 1.35 mL/hr

x kg or 70 mL/hr in a 50 kg pt, 100 mL/hr in 70 kg patientStable patients may be corrected with oral hydration

No consensus on management of pts w/ hypernatremia due to correction of hyperglycemia.

Slide66

HypoNatremia

Relative excess in water. Induced by marked inc. in H20 consumption (Polydipsia) and/or impaired H20 excretion r/t advanced renal failure or persistent release of ADH.Acute: developed over 48 hours. Usually from parenteral fluid admin. In postop patients (ADH assoc. w/ surgery), self-induced H20 intoxication (comp. runners, psychotic patients w/ extreme polydipsia, or ecstasy use).

Chronic

: persistent >48 hours or duration unclear.

Slide67

Hyponatremia

CLASSIFICATIONMild: serum sodium 130-134 mEq/LModerate: serum sodium 120-129 mEq/LSevere: serum sodium <120 mEq/LComplications from untreated or overcorrection are most common

Manifestations

Generally reflect the severity of cerebral

overhydration

Nausea and Malaise (earliest findings) seen when levels below 125-130

Headache, lethargy,

obtundation

, seizures, coma, respiratory arrest if levels below 115-120.

Noncardiogenic

pulmonary edema may also occur.

Acute

hyponatremic

encephalopathy may be reversible, but permanent neurological damage or death can occur, esp. in premenopausal women.

Slide68

Management of hyponatremia

Prevent further decline, dec. ICP for pts at risk for herniation, relieve symptoms, avoid excessive overcorrection.Even mild symptoms in acute hyponatremia present a medical emergency requiring aggressive treatment.Hypertonic Saline to prevent brain herniation.Mild: serum sodium 130-134): DO NOT treat with hypertonic saline. D/c causes, water restriction.

Asymptomatic:

sodium <130: 50 mL bolus 3% saline,

remeasure sodium every 1-2 hours.Symptomatic (even mild): sodium <130 w/ sx due to ICP, treat with 100 mL bolus 3% saline followed by up to 2 additional 100 mL doses if

sx continue. Bolus admin over 10 minutes.DO NOT USE Mannitol (nephrotoxic can lower Na- further) or Vasopressin antagonists (variable efficacy)Fluid Restriction of 50-60% daily fluid requirements; typically 800 mL/day restriction.Oral salt tablets, Loop Diuretics, K+ replacement for chronic hyopnatremia

Slide69

fatigue

Fatigue: is difficulty or inability to initiate and maintain activity . Acute fatigue - one month or less.Subacute fatigue - one to six months. Chronic fatigue - lasting over six months. 

Causes for fatigue that can be

diagnosed with stat BMP are-

Electrolyte abnormalities

Acute or chronic renal diseaseMedication toxicity

Slide70

When You do Not want to use POC BMP in CLINIC

Altered Mental StatusPyelonephritisAcute AbdomenNVD that just beganDo not use POC BMP if the results will not change your management or treatment plan.Do not use this test if you are already planning to send the patient to the ER. I.E. AMS, DKA, EKG changes with active CP.

Slide71

Pediatrics

Use BMP sparingly in pediatric Urgent Care setting:Healthy children without chronic disease should not have significant findings during an acute illnessIll appearing children who warrant evaluation of electrolytes will  need further evaluation in the ED regardless of the

results.

Slide72

Pediatrics-INdications for BMP

Dehydration-for young children hydration will likely occur in the ED. This could be further discussed as we expand our pediatric services. Suspected accidental ingestion-Follow Poison Control guideline

Mental Status Changes

-evaluate in ED

New Onset Seizure-evaluate in EDTick Born Disease-by the time they have hyponatremia patients are ill appearing and need to be evaluated in ED

Slide73

Pediatrics-INdications for BMP

DKA-To EDNew Onset Diabetes-work closely with endocrine or to ED

EKG changes

- such as large pointed T-waves, likely to ED

Hematuria with "Coco-Cola" Urine-This is reasonable to evaluate in UC to look for PSGN. Check BP. Discuss with Nephrology. Close follow up if discharged

Feeding Problems/Behavioral changes in infant: Infants and toddlers with metabolic disease may present with nonspecific findings, especially with their first viral illness or initiating formula/fructose.  Will often be hypoglycemic and low Bicarb

Slide74

Pediatrics-Normal variations

Review age specific normal valuesBlood Glucose: lower in infants and children 

BUN and Creatinine

: Lower due to less muscle mass

Potassium: a little higher in infants as kidneys lless efficient and excreting potassium

Slide75

resources

-Up to Date-Pediatric

Christopher Fink, DO

Assistant Professor of Medicine, Duke University School of Medicine

Duke Primary Care Medical Director for Clinical Laboratory Practice

Internal MedicineChristopher.D.Fink@Duke.edu616-283-0322