workshop case for fluid and electrolyte disorders

SUBSECTION D3FACILITATOR: DRA. COMES -

NATIVIDAD

R I V E R E . R O B O S A . R O D A S. R O D R I G U E Z. R O G EL I O. R O Q U E . R UA N T O. S A B A LVA R O.

S A L A C. SA L A Z A R , J. S A L A Z A R , R . S A L C E D O

WORKSHOP CASE FOR FLUID AND ELECTROLYTE

DISORDERS

Hyponatremia

1 week PTA •Fever, dysuria, urgency•Took Paracetamol and antibiotic which relieved fever

2 days PTA •Headache, body malaise, nausea, vomited 3x (50 cc/episode)

Admission •Persistence of symptoms

51 year old, femaleCC: vomiting

HistoryROS unremarkable

(-) for smoking and alcohol history

Physical Examination

JVP <5cm H20 at 45 degrees

Laboratory Tests

Hb=132 mg/dL Hct=0.35 WBC=12.5

Neutrophils=0.88Lymphocytes=0.12

P Na=123 mEq/L P K=3.7 mEq/L (N)

Cl=71 mEq/LBUN=22 mg/dL

S Crea=0.9 mg/dLGlucose=98 mg/dL

ABG:pH=7.3CO2=35

HCO3=18

U Na=100 mmol/LU Osm=540 mosm/L

Urinalysis:Yellow, sl.turbid

pH 6.0, SG 1.020albumin and sugar (-)

hyaline casts 5/hpfpus cells 10-15/hpfRBC 2-5/hpf (not

dysmorphic)

Salient Features

51 year old, female • Vomiting• Fever, dysuria, urgency• Headache, body malaise, nausea• Vomiting: 50cc/episode• Known hypertensive

• Telmisartan (40 mg)• Hydrochlorthiazide (12.5 daily)

• Weak looking, wheelchair-borne• BP: 120/80 (supine), 90/60 (sitting), 130/80 (usual)• HR: 90/min (supine), 105/min (sitting)• Lost weight, poor skin turgor, dry mouth, tongue and axillae• Normal JVP

1. What is the diagnosis? Basis?

Hypoosmolal hyponatremia secondary to thiazide intake

Body malaise

Weakness

Poor skin turgor

Dry mouth and tongue

Dry axillae

Postural hypotension

Postural tachycardia

Signs of ECF Volume Contraction

2. What factors contributed to the development of

hyponatremia in the patient?

Factors in the Development of Hyponatremia

Vomited 3x (50 cc/episode) Primary Sodium Loss (Secondary water gain):

GastointestinaI Losses Due to vomiting predisposes the patient to hyponatremia

since there is a corresponding sodium loss associated with water loss


Intake of hydrochlorothiazide Primary Sodium Loss (Secondary water gain): Renal

Losses It is important to note that diuretic-induced

hyponatremia is almost always due to thiazide diuretics lead to Na+ and K+ depletion and AVP-mediated water retention.

Inhibits reabsorption of sodium and chloride in the distal convoluted tubule promoting water loss.


Intake of telmisartan ARB

Inhibits tubular Na and Cl reabsorption, K excretion, water retention promotes water loss.

3. Compute for the plasma osmolality and the effective plasma osmolality. What is the importance

of computing for such?

Plasma Osmolality and Effective Plasma Osmolality

Osmolality (calc) = 2 x Na + glucose + urea**if all measurements in mmol/L

Osmolality (calc) = 2 x Na + glucose/18 + urea/2.8**if measurements are in mg/dL

Given: Plasma Na = 123 mEq/L Glucose = 98 mg/dL Urea = 22 mg/dL

Osmolality = 2(123) + (98/18) + (22/2.8) Osmolality = 259. 301N = 275 – 295 milli-osmoles per

kilogramReference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.

< 275 = Hyponatremia

Plasma Osmolality and Effective Plasma Osmolality

Effective Osmolality (calc) = 2 x Na + glucose**if all measurements in mmol/L

Osmolality (calc) = 2 x Na + glucose/18**if measurements are in mg/dL

Given: Plasma Na = 123 mEq/L Glucose = 98 mg/dL Urea = 22 mg/dL

Osmolality = 2(123) + (98/18)Osmolality = 251.44

Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.

Importance of computing for the plasma osmolality and the effective plasma osmolality

ECF tonicity is determined primarily by the Na+ concentration and patients who have hyponatremia have a decreased plasma osmolality.

Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.

4. What are the significance of urine osmolality (Uosm) and

urine sodium (Una)?

Urine Osmolality (Uosm)

• A more exact measurement of urine concentration than specific gravity– Patient with Uosm below 100 mOsm/kg are able to

appropriately suppress ADH release, leading to a maximally dilute urine

– Patients with a higher urine osmolality have an impairment in water excretion due to the presence of ADH

• Indicated to evaluate the concentrating and diluting ability of the kidney • Accurate test for decreased kidney function • Monitor course of renal disease/ electrolyte therapy

Reference: Rennke H., Denker, B. 2007. Renal Pathophysiology: The Essentials

Urine Sodium (UNa)

• Helps distinguish renal from nonrenal causes of hyponatremia

• Urine sodium exceeding 20 mEq/L is consistent with renal salt wasting.– Diuretics, ACE inhibitors, mineralocorticoid deficiency,

salt losing nephropathy

• Urine sodium less than 10 mEq/L implies avid sodium retention by the kidney.– Compensation for extra-renal fluid loss (vomiting,

diarrhea, sweating or third space wasting)



Urine Sodium (UNa)

• Effective circulating volume depletion and SIADH are the two major causes of true hyponatremia (with an inappropriately high urine osmolality) and these disordes can be distinguished by measuring the Una.

– Patients with hypovolemia are sodium avid in an attempt to limit further losses.

• Urine sodium is generally below 25 mEq/L.

– In comparison, patients with SIADH are normovolemic and sodium excretion is in a steady state equal to intake.

• Urine sodium concentration is typically above 40 mEq/L.

5. Compute for the sodium (Na) deficit.

Na deficit

Sodium Deficit = Total Body Water * Normal Wt in kg * (Pt's Na - Desired Na)

(TBW = 0.6 if male and 0.5 if female)

Na deficit

Sodium Deficit = (0.5)* (53kg)* (135mEq/L-123mEq/L)

Sodium Deficit= 318mmol/L

Principles of Therapy

Raise plasma sodium concentration by restricting water intake and promoting water loss.

Correct underlying disorder.

6. What are the basic principles in the treatment of

hyponatremia?


Asymptomatic hyponatremia Sodium repletion (isotonic saline) Restoration of euvolemia removes the hemodynamic

stimulus for AVP release. Restriction of sodium and water intake, correction of

hypokalemia, and promotion of water loss in excess of sodium.

Dietary water restriction should be less than urine output.


Asymptomatic Hyponatremia Sodium concentration should be raised by no more

than 0.5 – 1.0mmol/L over the first 24 hours.Acute or severe Hyponatremia

Plasma sodium conc: < 110-115mmol/L Rapid correction

Severe symptomatic Hypertonic saline 1-2 mmol/l per hour for the first 3-4 hours Raised by no more than 12mmol/L during the first 24

hours

7. What is the complication of the rapid correction of the

hyponatremia?

Complication of Rapid Correction of Hyponatremia

Rate of correction: depends on the absence or presence of neurologic dysfunction Related to the rapidity of onset and magnitude of fall

in plasma Na+ concentrationRapid correction of hyponatremia leads to

osmotic demyelination syndrome (ODS).

Osmotic Demyelination Syndrome

Neurologic disorder characterized by flaccid paralysis, dysarthria and dysphagia

Mechanism:Patients with chronic

hyponatremia (brain cell volume has

returned to near normal)

Sudden osmotic shrinkage of brain cells

Prior cerebral anoxic injury

Hypokalemia

Malnutrition secondary to alcoholism

Administration of hypertonic

saline

References: Vellaichamy M. Hyponatremia. 2009. http://emedicine.medscape.com/article/907841-followup. Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.

May re

sult i

n

br

ai

n

damage

and

deat

h

Central Pontine Myelinolysis

References: Vellaichamy M. Hyponatremia. 2009. http://emedicine.medscape.com/article/907841-followup. Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed. Schwartz’s Principles of Surgery, 8th ed.

Central Pontine Myelinolysis

Predilection for pons:

During hyponatremia, these cells can adapt only by losing ions instead of swelling. This limitation makes them prone to damage when Na is replaced.

Grid arrangement of the oligodendrocytes in the base of pons

Limits their mechanical flexibility, thus capacity to swell

Reference: Vellaichamy M. Hyponatremia. 2009. <http://emedicine.medscape.com/article/907841-followup>

Central pontine myelinolysis, MRI FLAIR

T2 weighted magnetic resonance scan image showing bilaterally symmetrical

hyperintensities in caudate nucleus (small, thin arrow), putamen (long

arrow), with sparing of globus pallidus (broad arrow), suggestive of extrapontine myelinolysis.

8. What intravenous fluid would you use? At what rate should it

be given?

Intravenous fluid to use and rate of infusion

3% saline infused at a rate of ≤ 0.05 mL/kg body weight per minute.

Effect should be monitored continuously by STAT measurements of serum sodium at least once every 2 hours.

Reference: Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.

Intravenous fluid to use and rate of infusion

Infusion should be stopped as soon as serum sodium increases by 12 mmol/L or to 130 mmol/L, whichever comes first.

Urine output should be monitored continuously. SIAD can remit spontaneously at any time, resulting in

an acute water diuresis that greatly accelerates the rate of rise in serum sodium produced by fluid restriction and 3% saline.

Reference: Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.

Hyperkalemia

A 62 y/o M diabetic with chronic kidney disease and a creatinine of 3.5 mg/dl and an estimated GFR of 15 ml/min consults due to the inability to lift himself from a

chair. He had been eating fruits with each meal for the past two weeks. On PE there is marked proximal weakness and

decreased skin turgor. The ECG revealed peaked T waves and widening of the P

wave and QRS complex.

Salient Features

62, MCKDDiabeticCC: inability to lift himself from a chairCreatinine of 3.5 mg/dlGFR of 15 ml/min – LowDecreased skin turgor and marked proximal

weaknessECG: Peaked T waves and widening of P wave

and QRS complex

Laboratory Results

Parameters Patient Normal Values

Plasma Na 130 meq/L 136-146 meq/L

K 8.5 meq/L 3.5-5.0 meq/L

Cl 98 meq/L 102-109 meq/L

HCO3 17 meq/L 22-30 meq/L

Creatinine 2.7 meq/L 0.6-1.2 meq/L

pH 7.32 7.35-7.45

Capillary Blood Glucose

400 mmol/L 3.9-6.7 mmol not more than 125 mg/dl

Serum Acetone + -

1. What are the most likely factors responsible for the elevation of

the plasma potassium?

Most likely causes of Hyperkalemia in the patient

1. ) The patient has chronic kidney disease and is in renal failure – GFR 15 ml/min Compensatory mechanism for increasing distal flow

rate and K secretion per nephron is decreased because there is decreased renal mass in chronic renal insufficiency

2.) The patient has diabetes- Insulin deficiency and hypertonicity promote K shift from the ICF to the ECF.

3. Intake of fruits does not necessarily cause hyperkalemia.

- Huge amount of parenteral K can elicit hyperkalemia.

4. Acidosis causes shift of potassium from intracellular space into extracellular space.

2. Is this pseudohyperkalemia? Why

or why not?

PSEUDOHYPERKALEMIA

Artificially elevated plasma K+ concentration due to K + movement out of cells immediately prior to or following venipuncture

Contributing factors: prolonged use of tourniquet with or without repeated fist clenching, hemolysis, and marked leukocytosis or thrombocytosis

marked leukocytosis or thrombocytosis results in an elevated serum K + concentration due to release of intracellular K + following clot formation

References: Harrison’s Principles of Internal Medicine 17th ed. Onyekachi Ifudu, Mariana S. Markell, Eli A. Friedman. Unrecognized Pseudohyperkalemia as a Cause of Elevated Potassium in Patients with Renal Disease.

PSEUDOHYPERKALEMIA

Serum to plasma potassium difference of more than 0.4 mmol/l

Occurs when platelets, leukocytes or erythrocytes release intracellular potassium in vitrofalsely elevated serum values.

Observed in: Myeloproliferative disorders including leukemia Infectious mononucleosis Rheumatoid arthritis

NO… THIS IS NOT PSEUDOHYPERKALEMIA SINCE THERE ARE NO ENOUGH EVIDENCE OF BLOOD COUNT

DIFFERENTIALS AS WELL AS NO HISTORY PREDISPOSING THE PATIENT TO DEVELOP SUCH.

ALSO, THE PRESENCE OF ECG ABNORMALITIES WHICH REQUIRE EMERGENCY THERAPY IS NOT A COMMON

INDICATION IN PSEUDOHYPERKALEMIA.

2. Is this pseudohyperkalemia? Why

or why not?

3. What are the clinical manifestations of hyperkalemia in

this patient? Explain the pathophysiology.

HYPERKALEMIA

Excessive intake Uncommon cause of hyperkalemia Most often, hyperkalemia is caused by a relatively

high potassium intake in a patient with impaired mechanisms for the intracellular shift of potassium or for renal potassium excretion

Decreased excretion Most common cause of hyperkalemia

Decreased excretion of potassium, especially coupled with excessive intake

Decreased renal potassium excretion Renal failure Ingestion of drugs that interfere with potassium excretion

Potassium-sparing diuretics, angiotensin-convening enzyme inhibitors, nonsteroidal anti-inflammatory drugs

Impaired responsiveness of the distal tubule to aldosterone Type IV renal tubular acidosis observed with diabetes

mellitus, sickle cell disease, or chronic partial urinary tract obstruction

Shift from intracellular to extracellular space Uncommon cause of hyperkalemia Exacerbate hyperkalemia produced by a high intake

or impaired renal excretion of potassium. Clinical situations in which this mechanism is the

major cause of hyperkalemia includes Hyperosmolality Rhabdomyolysis Tumor lysis Succinylcholine administration

Depolarizes the cell membrane and thus permits potassium to leave the cells

CLINICAL MANIFESTATIONS

Weakness Prolonged depolarization impairs membrane

excitability Since the resting membrane potential is related to the

ratio of the ICF to ECF K+ concentration, hyperkalemia partially depolarizes the cell membrane

It may progress to flaccid paralysis and hypoventilation if the respiratory muscles are involved

Metabolic acidosis Net acid excretion is impaired

Inhibition of renal ammoniagenesis and reabsorption of NH4

+ in the TALH It may exacerbate the hyperkalemia due to K+

movement out of cells

Cardiac toxicity Increased T-wave amplitude, or peaked T waves Prolonged PR interval and QRS duration,

atrioventricular conduction delay, and loss of P waves More severe degrees of hyperkalemia

Sine wave pattern Progressive widening of the QRS complex and merging

with the T wave The terminal event is usually ventricular fibrillation or

asystole

How would you manage this case?

Management

Most important consequence of Hyper K is altered Cardiac Conductance With the risk of bradycardia and cardiac arrest

The patient should be treated as an emergency case and warrants emergency treatment + ECG changes and K > 6.0 mM (Px= 8.5 mM)

Urgent Management

12- lead ECGAdmission to the hospitalContinuous cardiac monitoringImmediate treatment

Treatment

Antagonism of the cardiac effect of hyperkalemia Stabilize membrane potential

Calcium Therapy 10% Ca gluconate, 10 mL over 10 mins or Calcium chloride 5 mL of 10% sol IV over 2 min

Stop infusion if bradycardia developsRapid reduction in K+ by redistribution into

cells Cellular K+ uptake

Insulin 10 U R (CBG= 400 mmol/L) B2-agonist nebulize albuterol, 10-20 mg in 4mL saline

Treatment

Removal of K+ from the body Furosemide 20-250 mg IV Kayexalate 30-60 g mixed with 100 mL of 20% sorbitol

PO Hemodialysis (if necessary)

Intractable Acidosis Uncontrollable Hyperkalemia

Sodium Bicarbonate 1 mEq/kg slow IV push or continuous IV drip

Hypokalemia

History

A 55 year old man presents with diarrhea that has lasted for several weeks. He works as a farmer in La Trinidad, Benguet. He has become progressively weak during the past week.

Laboratory Examination

Laboratory examination reveals the following results: Na = 140 mEq/LCl = 110 mEq/LK = 2.0 mEq/LAn arterial blood gas determination shows:pH = 7.28pCO2 = 39 mmHgHCO3 = 16The urine potassium is 15 mEq/L.

1. Discuss the diagnostic approach to hypokalemia. What is the cause

of hypokalemia in this patient?

HYPOKALEMIA

Decreased Intake

Redistribution into cells Increased Loss

Nonrenal

Gastrointestinal Loss (Diarrhea)

Integumentary Loss(Sweat)

Renal

Hypokalemia Secondary to Profuse Diarrhea

Increased gastrointestinal lossLoss of gastric secretions does not account for the

moderate to severe K+ depletion.The hypokalemia is primarily due to increased renal K+

excretion.Loss of gastric contents volume depletion and metabolic

alkalosis kaliuresisHypovolemia Aldosterone release Augmentation of K+

secretion by principal cellsThe filtered load of HCO3

– exceeds the reabsorptive capacity of the proximal convoluted tubule, thereby increasing distal delivery of NaHCO3, which enhances the electrochemical gradient favoring K+ loss in the urine.

2. What are the signs and symptoms of hypokalemia?

Symptoms

• Seldom occur unless the plasma K+ conc is <3mmol/L• Fatigue, myalgia, and muscular weakness of the

lower extremities• Palpitations, constipation, nausea or vomiting,

abdominal cramping, polyuria, nocturia, or polydipsia, psychosis, delirium, or hallucinations, depression

• Severe hypokalemia may lead to progressive weakness, hypoventilation and eventually complete paralysis.

• Hypokalemic periodic paralysis

Signs

• Signs of ileus• Hypotension• Ventricular arrhythmias• Cardiac arrest• Bradycardia or tachycardia• Premature atrial or ventricular beats• Hypoventilation, respiratory distress• Respiratory failure• Lethargy or other mental status changes• Decreased muscle strength, fasciculations, or tetany• Decreased tendon reflexes• Cushingoid appearance (eg, edema)

3. What are the adverse medical implications of this condition?

Hypokalemia

Impaired muscle metabolism and blunted hyperemic response to exercise associated with profound K+

depletion increase the risk of rhabdomyolysisSmooth muscle function may also be affected and

manifest as paralytic ileusECG changes:

Early changes: T wave flattening or inversion, prominent U wave, ST segment depression, prolonged QU interval

Severe K+ depletion: prolonged PR interval, decreased voltage and widening of QRS complex, and an increased risk of ventricular arrythmias (px with Myocardial Ischemia or left ventricular hypertrophy)

Hypokalemia

Predispose to digitalis toxicityAssociated with acid-base disturbances related to

the underlying disorderIntracellular acidification and an increase in net

acid excretion or new HCO3- production:

consequence of enhanced proximal HCO3-

reabsorption, increased renal ammoniagenesis, and increased distal H + secretion → generation of metabolic alkalosis

Glucose intolerance attributed to either impaired insulin secretion or peripheral insulin resistance.

4. What is the significance of the urinary K levels?

• Normal – Urine Potassium:25 to 120 mEq/L/day

• Increased – Primary or Secondary Aldosteronism– Glucocorticoids– Alkalosis– Renal Tubular Necrosis– Excess Potassium intake

• Decreased – Acute Renal failure– Potassium sparing diuretics– Diarrhea– hypokalemia

Decreased urine K levels (15mEq/L)

• Diarrhea for several weeks• Hypokalemia secondary to increased GI loss• 90% of K is reabosrbed by the PCT and loop of

Henle• Luminal Na K Cl co transporter mediated K

uptake in thick ascending loop• K delivery to the distal nephron (DCT and CCD)

approximates dietary intake• Net distal K secretion or reabsorption occurs in

the setting of K excess or depletion respectively

5. What is the treatment?

Emergency Department CarePatients in whom severe hypokalemia is suspected

should be placed on a cardiac monitor; establish intravenous access and assess respiratory status.

Direct potassium replacement therapy by the symptomatology and the potassium level. Begin therapy after laboratory confirmation of the diagnosis.

Patients who have mild or moderate hypokalemia (potassium level of 2.5-3.5 mEq/L) are usually asymptomatic; if these patients have only minor symptoms, they may need only oral potassium replacement therapy.

Patients with mild hypokalemia whose underlying cause of hypokalemia can be corrected may not need any potassium replacement, such as those with vomiting successfully treated with antiemetics. Reference: http://emedicine.medscape.com/article/767448-treatment

In severe hypokalemia, cardiac arrhythmias or significant symptoms are present, then more aggressive therapy is warranted.

If the potassium level is less than 2.5 mEq/L, intravenous potassium should be given. Admission or ED observation is indicated; replacement therapy takes more than a few hours.

The serum potassium level is difficult to replenish if the serum magnesium level is also low. Look to replace both.

Reference: http://emedicine.medscape.com/article/767448-treatment

Emergency Treatment

According to, August 2009 Journal:Emergency Treatment of Hypokalemia

A. Estimated Potassium Deficit1. At a serum K <3 mEq/L, there is a K deficit of more than 300 mEq2. At a serum K <2 mEq/L, there is a K deficit of more than 700 mEq

B. Indications for Urgent Replacement. Electrocardiographic abnormalities consistent with severe K

depletion, myocardial infarction, hypoxia, digitalis intoxication, marked muscle weakness, or respiratory muscle paralysis.

Reference: http://www.ccspublishing.com/journals2a/hypokalemia.htm

Emergency Treatment

C. Intravenous Potassium Therapy1. Intravenous KCL is usually used unless concomitant hypophosphatemia is present (diabetic ketoacidosis), where potassium phosphate is indicated. 2. The maximal rate of intravenous K replacement is 30 mEq/hour. The K concentration of IV fluids should be 40 mEq/L or less if given via a peripheral vein. Frequent monitoring of serum K and constant electrocardiographic monitoring are required.


Non-Emergent Treatment of Hypokalemia

Attempts should be made to normalize K levels if <3.5 mEq/L.

Oral supplementation is significantly safer than IV. Micro-encapsulated and sustained-release forms of KCL are less likely to induce gastrointestinal disturbances than are wax-matrix tablets or liquid preparations.

1. KCL elixir, 1-3 tablespoon every day.


References

Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.

Harrison’s Principle of Internal Medicine, 17th ed. Onyekachi Ifudu, Mariana S. Markell, Eli A. Friedman. Unrecognized

Pseudohyperkalemia as a Cause of Elevated Potassium in Patients with Renal Disease.

Rennke H., Denker, B. 2007. Renal Pathophysiology: The Essentials Schwartz’s Principles of Surgery, 8th ed. Vellaichamy M. Hyponatremia. 2009.

<http://emedicine.medscape.com/article/907841-followup> http://www.benhhoc.com/post/1816/ http://en.wikipedia.org/wiki/Orthostatic_hypotension http://www.mt911.com/site/lab/normal_lab_values.asp http://www.ccspublishing.com/journals2a/hypokalemia.htm http://emedicine.medscape.com/article/767448-treatment

workshop case for fluid and electrolyte disorders

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