GENERAL DATA Name: F.H.S. Age: 73 Sex: F Address: Tondo, Manila Occupation: None Religion: Roman Catholic CC: generalized body weakness.

GENERAL DATA

Name: F.H.S.Age: 73Sex: FAddress: Tondo, ManilaOccupation: NoneReligion: Roman CatholicCC: generalized body weakness

HISTORY OF PRESENT ILLNESS

3 days PTA:-generalized weakness (difficulty getting up from bed, feeling of falling when ambulating-headache, nausea & vomiting (3episodes)-loss of appetite-hospital: BP 190/100, meds: Clonidine 75mg/tab sublingual

2 days PTA:- persistent generalized weakness-1 episode of vomiting-incoherence

Admission

REVIEW OF SYSTEMS• Review of Systems• No weight loss• Wears glasses• (+) decreased hearing acuity, No ear pain, discharge or tinnitus• No sore throat, oral sores• No neck masses, no limitation of motion• No difficulty of breathing• (+) nocturia, frequency, (-) dysuria, (-) oliguria• (+) polyuria, polydipsia • No tremors, no heat or cold intolerance• No seizures, syncope• No joint pains, no joint stiffness, no swelling• No easy bruisability

PAST MEDICAL HISTORY

• (+) Hypertension (1987) medication: Losartan+hydroclorothiazide 100mg/12.5mg tab OD and Amlodipine 10mg/tab OD

• (+) 2007 – hospitalized for multiple electrolyte imbalance secondary to GI losses secondary to AGE

• (-) DM, CVA, Asthma, Allergy, CA, PTB

FAMILY HISTORY

• (+) Hypertension – father, siblings• (+) renal disease – sibling• (-) Diabetes Mellitus• (-) PTB • (-) Cancer

PERSONAL AND SOCIAL HISTORY

• Non Smoker• Non Alcoholic beverage drinker • No illicit drug use• Diet: prefers salty foods

PHYSICAL EXAMINATION• Conscious, coherent, asthenic, well-kempt, ambulatory with assistance, not in

cardiopulmonary distress• VS: BP: 120/70 PR 69 bpm, RR 24 cpm, T 36.3 °C • Wt 56kg Ht 152.4 BMI 23.93 • Warm moist skin with no active dermatoses• Pink palpebral conjunctiva, anicteric sclera, pupils 2-3 mm ERTL, (+) arcus senilis OU• No tragal tenderness, no nasoaural discharge, nasal septum midline• Moist buccal mucosa, non-hyperemic posterior pharyngeal wall, tonsils not enlarged• Supple neck, no palpable cervical lymph nodes, thyroid gland not enlarged• Symmetrical chest expansion, no lagging, no retractions, resonant on percussion, clear

breath sounds on both lung fields• Adynamic precordium, no heaves, lifts and thrills, AB at 6th LICS AAL, S1 > S2 at apex, S2 > S1

at base, no murmurs• Abdomen flabby, NABS, no bruits, no masses, no guarding, nontender, tympanitic on

percussion, liver not enlarged, (-) CVA tenderness• Pulses full and equal, no edema, no cyanosis

Neurological Exam• Conscious, coherent, can follow commands. GCS 15 E4V5M6• Cranial nerves: • CN I (-) anosmia• CN II intact papillary light reflex, and (+) ROR• CN III, IV, VI- EOMs full and equal• CN V- V1-V3 intact• CN VII- can raise eyebrows, can frown, can smile, can puff cheeks• CN VIII- decreased hearing acuity AU• CN IX, X- uvula midline on phonation• CN XI- can raise shoulders against resistance• CN XII- tongue midline uvula is in the midline on protrusion• MMT 5/5 on all extremities• No sensory deficits• Cerebellar function intact• (-) Babinski, (-) Nuchal rigidity, (-) Kernigs, (-) Brudzinski

ASSESSMENT

• Electrolyte imbalance secondary to 1.) GI loss 2. diuretic use 3. herbal use

• Hypertension St. II• Urinary tract Infection

PLAN• Plan:• Diagnostic• CBC c platelet,• CBG• Na, K• Plasma Osmolality• Urine Osmolality• Na Urine• K Urine• Urinalysis

CBC c Platelet Reference Range 7/21Hgb 120-170 124RBC 4.0-6.0 4.36Hct 0.37-0.54 0.37

MCV 87±5 84.10MCH 29±2 28.40

MCHC 34±2 33.70RDW 11.6-14.6 14.10MPV 7.4-10.4 5.60

Platelet 150-450 295WBC 4.5-10.0 11.00

Neutrophils 0.65

Metamyelocytes -

Bands -

Segmented 0.65

Lymphocytes 0.34

Monocytes -

Eosinophils 0.01

Basophils -

Chemistry Reference Range

7/20 7/21 7/22

BUN 9-23 8.39Creatinine 0.5-1.2 0.72

Sodium 137-147 119.84 124.00/131.79 135.00

Potassium 3.8-5 3.73 3.48/3.48 3.93

Plasma Osmolality

280-295 275.00

Urine Sodium 40-220 13.00

Urine Potassium

25-125 4.30

Urine Osmolality

500-800 92.00

FBS 70.9-110 111.41

Urinalysis 7/21Color light yellow, Transparency turbid, pH 7.0, Specific gravity 1.005, Albumin (-), Sugar (-), RBC 20-30/hpf, Pus over 100/hpf, Squamous cells few, Bacteria ++++, Mucus threads few

Chest X-ray (Official) 7/21The heart is enlargedAorta is calcifiedThe pulmonary vascularity is normalThe diaphragm and sinuses are intactThe visualized osseous structures are unremarkableIMPRESSION: Cardiomegaly, Atheromatous aorta

Urine Gram stain 7/21No microorganisms seen on both centrifuged and uncentrifuged sample

Urine Culture 7/23/10No growth after 2 days of incubation

Potassium Balance

Haziel dela Rosa

Potassium

• major intracellular cation• plasma K+ concentration is 3.5–5.0 mmol/L• intacellular: 150 mmol/L• extracellular: 30–70 mmol – constitutes <2% of the total body K+ content (2500–

4500 mmol).• ratio of ICF to ECF K+ concentration – (normally 38:1) : due to resting membrane potential

• crucial for normal neuromuscular function

Potassium balance

– basolateral Na+, K+-ATPase pump actively transports K+ in and Na+ out of the cell in a 2:3 ratio

– passive outward diffusion of K+ • quantitatively the most important factor that generates

the resting membrane potential– Na+, K+-ATPase pump• Stimulated by increased intracellular Na+

concentration• Inhibited by:

– digoxin toxicity or chronic illness such as heart failure or renal failure

Potassium balance

• Maintenance of the steady state necessitates matching K+ ingestion with excretion

• extrarenal adaptive mechanisms, followed by urinary excretion– Prevents doubling of the plasma K+ concentration that

would occur if the dietary K+ load remained in the ECF compartment

• following a meal, most of the absorbed K+ enters cells– initial elevation in the plasma K+ concentration – facilitated by insulin release and basal catecholamine

levels

Potassium balance

• excess K+ is excreted in the urine • amount of K+ lost in the stool can increase

from 10 to 50% or 60% (of dietary intake) in chronic renal insufficiency

• colonic secretion of K+ is stimulated in patients with large volumes of diarrhea– severe K+ depletion

Potassium Excretion

• Renal excretion– major route of elimination of dietary and other

sources of excess K+

– filtered load of K+ (GFR x plasma K+ concentration = 180 L/d x 4 mmol/L = 720 mmol/d) is ten- to twentyfold greater than the ECF K+ content

Potassium Excretion

– 90% of filtered K+ is reabsorbed by the proximal convoluted tubule and loop of Henle

– Proximally, K+ is reabsorbed passively with Na+ and water

– luminal Na+-K+-2Cl– co-transporter mediates K+ uptake in the thick ascending limb of the loop of Henle

Potassium Excretion• K+ delivery to the distal nephron [distal

convoluted tubule and cortical collecting duct (CCD)]– approximates dietary intake

• Net distal K+ secretion or reabsorption occurs in the setting of K+ excess or depletion, respectively.

• principal cell – responsible for K+ secretion in the late distal

convoluted tubule (or connecting tubule) and CCD• Virtually all regulation of renal K+ excretion and

total body K+ balance occurs in the distal nephron

Potassium Excretion

• secretion is regulated by two physiologic stimuli– aldosterone and hyperkalemia

• Aldosterone– secreted by the zona glomerulosa cells of the

adrenal cortex in response to high renin and angiotensin II or hyperkalemia

– plasma K+ concentration, independent of aldosterone, can directly affect K+ secretion

Potassium Excretion

Aldosterone– K+ concentration in the lumen of the CCD, renal K+

loss depends on the urine flow rate, a function of daily solute excretion

– increased distal flow rate can significantly enhance urinary K+ output

– severe K+ depletion• secretion is reduced and reabsorption in the cortical

and medullary collecting ducts is upregulated.

Estimation of Potassium Deficit

• For a fall in serum potassium from 4.0 to 3.0 meq/L, body potassium deficit is 200-300 meq/70 kg BW

• For a serum potassium at 2.5 meq/L, body deficit is 500 meq/70 kg BW

• For a serum potassium at 2.0 meq/L, body deficit is 700 meq/70 kg BW

In the patient....Reference

value7/20 7/21 7/22 Potassium

Deficit

Serum Potassium

3.8-5 3.73 LOW 3.48/3.48 LOW

3.93 200-300 meq/70 kg

BW

Urine Potassium

25-125 4.30 LOW

Plasma Osmolality

280-295 275.00 LOW

Urine Osmolality

500-800 92.00 LOW

Clinical Features of Hypokalemia

Hypokalemia• Symptoms seldom occur unless the plasma K+

concentration is <3 mmol/L. • Fatigue, myalgia, and muscular weakness of

the lower extremitieslower (more negative) resting membrane potential.

• More severe hypokalemia :– progressive weakness,– hypoventilation (due to respiratory muscle

involvement),– complete paralysis.

• Increase risk of rhabdomyolysis

Electrographic changes of hypokalemia

• Early changes:– flattening or inversion of the

T wave, – a prominent U wave– ST-segment depression,– a prolonged QU interval.

• Severe K+ depletion:– prolonged PR interval– decreased voltage and

widening of the QRS complex, – increased risk of ventricular

arrhythmias, especially in patients with myocardial ischemia or left ventricular hypertrophy.

Etiology of Hypokalemia

CAUSES OF HYPOKALEMIAI. Decreased Intake

A) starvationB) clay ingestion

II. Redistribution into the cellsA) Acid-Base

1) Metabolic AlkalosisB) Hormonal

1) Insulin2) B2-Adrenergic agonists3) Alpha-Adrenergic antagonists

C)Anabolic state1) Vitamin B12 or folic acid 2) Granulocyte-macrophage colony stimulating factor 3) Total parenteral nutrition

D) Others1)Pseudohypokalemia2)Hypothermia3)Hypokalemic periodic paralysis4)Barium toxicity

CAUSES OF HYPOKALEMIA

III. Increased lossA) Nonrenal

1. Gastrointestinal loss (diarrhea)2. Integumentary loss (sweat)

B) Renal 1. Increased distal flow: diuretics, osmotic diuresis, salt-wasting nephropathies2. Increased secretion of potassium

2) Increased secretion of potassium

A. Mineralocorticoid excess: primary hyperaldosteronism, secondary hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal artery stenosis, hypovolemia), apparent mineralocorticoid excess (licorice, chewing tobacco, carbenoxolone), congenital adrenal hyperplasia, Cushing's syndrome, Bartter's syndrome

B. Distal delivery of non-reabsorbed anions: vomiting, nasogastric suction, proximal (type 2) renal tubular acidosis, diabetic ketoacidosis, glue-sniffing (toluene abuse), penicillin derivatives

C. Other: amphotericin B, Liddle's syndrome, hypomagnesemia

Hyponatremia

Causes of Hyponatremia

I. PseudohyponatremiaA. Normal plasma osmolality

1. Hyperlipidemia2. Hyperproteinemia3. Posttransurethral resection of prostate/bladder

B. Increased plasma osmolality1. Hyperglycemia2. Mannitol

Causes of Hyponatremia

II. Hypoosmolal hyponatremiaA. Primary Na loss (secondary water gain)

1. Integumentary loss: sweating, burns2. GI loss: vomiting, tube drainage, fistula, obstruction, diarrhea

B. Primary water gain (secondary Na loss)1. Primary polydipsia2. Decreased solute intake3. AVP release d/t pain, nausea, drugs4. SIADH5. Glucocorticoid deficiency6. Hypothyroidism7. Chronic renal insufficiency

Cause of Hyponatremia

C. Primary Na gain (exceeded by secondary water gain)

1. Heart failure2. Hepatic cirrhosis3. Nephrotic syndrome

Approach to the diagnosis of patients with hyponatremia

Four laboratory findings often provide usefulinformation and can narrow the differential

diagnosis of hyponatremia:(1)the plasma osmolality(2) the urine osmolality(3) the urine Na+ concentration(4) the urine K+ concentration

Approach to a Patient with Hyponatremia

275

92

• (-) urine osmolality and specific gravity of <100 mosmol/kg and 1.003- it suggests impaired free-water excretion due to the action of AVP on the kidney

• The secretion of AVP may be a physiologic response to hemodynamic stimuli or it may be inappropriate in the presence of hyponatremia and euvolemia

Hypokalemia: Treatment

• Kalium durule (750 mg/tab)1 durule TID x 4 doses

• Increase K in the diet

SIADH• hypoosmotic hyponatremia in the setting of an

inappropriately concentrated urine (urine osmolality >100 mosmol/kg).

• normovolemic and have normal Na+ balance. • urine Na+ excretion rate equal to intake (urine

Na+ concentration usually >40 mmol/L).• normal renal, adrenal, and thyroid function and

usually have normal K+ and acid-base balance.• associated with hypouricemia due to the

uricosuric state induced by volume expansion.

SIADH

• Most common causes: neuropsychiatric and pulmonary diseases, malignant tumors, major surgery (postoperative pain), and pharmacologic agents

• Adrenal insufficiency and hypothyroidism may present with hyponatremia and should not be confused with SIADH

ADRENAL INSUFFICIENCY

• Decreased mineralocorticoids contribute to the hyponatremia of adrenal insufficiency

• Cortisol deficiency hypersecretion of AVP both indirectly (secondary to volume depletion) and directly (cosecreted with corticotropin-releasing factor)

HYPOTHYROIDISM

• The mechanisms that lead to hyponatremia:– decreased cardiac output and GFR– increased AVP secretion in response to

hemodynamic stimuli

Basic Principles in the Treatment of Hyponatremia

Goals of Therapy

• (1) to raise the plasma Na+ concentration by restricting water intake and promoting water loss

• (2) to correct the underlying disorder.

• Mild asymptomatic hyponatremia no treatment• Asymptomatic hyponatremia associated with ECF

volume contraction– Na+ repletion with isotonic saline– Restoration of euvolemia removes the hemodynamic

stimulus for AVP release, allowing the excess free water to be excreted

Goals of Therapy• Hyponatremia associated with edematous states – Reflect severity of the underlying disease, usually

asymptomatic– Restriction of Na+ and water intake

• hyponatremia associated with primary polydipsia, renal failure, and SIADH

– Correction of hypokalemia• Correction of the K+ deficit may raise the plasma Na+

concentration by favoring a shift of Na+ out of cells as K+ moves in

– Non-peptide vasopressin antagonists new selective treatment for euvolemic and hypervolemic hyponatremia

Rate of Correction of Hyponatremia

• Depends on the absence or presence of neurologic dysfunction

• Asymptomatic patients– no more than 0.5–1.0 mmol/L per h and by less

than 10–12 mmol/L over the first 24 h• Acute or severe hyponatremia (plasma Na+

concentration <110–115 mmol/L) – altered mental status and/or seizures– requires more rapid correction.

Rate of Correction of Hyponatremia

• Severe symptomatic hyponatremia – Hypertonic saline– 1–2 mmol/L per hour for the first 3–4 h or until the seizures

subside– no more than 12 mmol/L during the first 24 h– quantity of Na+ required to increase the plasma Na+

concentration by a given amount can be estimated by multiplying the deficit in plasma Na+ concentration by the total body water

– Amount of mmol of Na+ needed to raise the plasma Na concentration from actual to desired = [(135 – actual) x BW x 0.5].

Rate of correction and Fluids

Cruz, Karen

What IV fluids should be used?At what rate should it be given?

• Asymptomatic patients:– Isotonic saline–Concentration should be raised by no more

than 0.5 to 1.0 mmol/L per hour and by less than 10 to 12 mmol/L over 1st 24 hr

• Acute/severe hyponatremia– Plasma Na concentration <110-115 mmol/L– Tends to present with altered mental status

and/or seizures– Requires more rapid correction

• severe symptomatic patients:–Hypertonic saline (3%)–Raised by 1 to 2 mmol/L per hr for the 1st 3-

4 hr or until seizure subsides–Raised by no more than 12mmol/L during

the first 24 hours

Different IV fluids and Na contentIV Fluids Na Content (mEq/L)

PNSS 154

LRS 130

0.9% NaCl 154

D5 0.45% NaCL 77

D5 3% NaCl 513

D5 5% NaCl 855

FLUIDS

• LRS and normal saline– Isotonic– useful in replacing gastrointestinal losses and

extracellular volume deficits

• Lactated Ringer's is slightly hypotonic– 130 mEq of sodium, which is balanced by 109 mEq

of chloride and 28 mEq of lactate

FLUIDS

• Sodium chloride– mildly hypertonic 154 mEq of Na+ balanced by

154 mEq of Cl-– an ideal solution for correcting volume deficits

associated with hyponatremia, hypochloremia, and metabolic alkalosis

FLUIDS• 0.45% sodium chloride– useful to replace ongoing gastrointestinal losses as

well as for maintenance fluid therapy in the postoperative period

– provides sufficient free water for insensible losses and enough sodium to aid the kidneys in adjustment of serum sodium levels

– 5% dextrose supplies 200 kcal/L, always added to solutions containing less than 0.45% sodium chloride to maintain osmolality prevent lysis of RBCs that may occur with rapid infusion of hypotonic fluids

FLUIDS

• Hypertonic saline solutions (3.5% and 5%)– used for correction of severe sodium deficits

Sodium Deficit

Na Deficit = (Desired Na – Actual Na) x TBW x weight (kg)– Actual Na: 119.84– Weight: 56 kg

=

= 0.45 x 56kg x (130-119.84)= (25.2) (10.16)

Sodium deficit = 256.03 mEq/L

Total body weight (in Liters)

Children 0.6 x weightWomen 0.5 x weightMen 0.6 x weightElderly Women 0.45 x weightElderly Men 0.5 x weight

Adrogue, HJ; and Madias, NE. Primary Care: Hypernatremia. New England Journal of Medicine 2000; 342(20):1493-1499. 342(21):1581-1589. .

Sodium Correction

Different IV fluids and Na content

IV Fluids Na Content (mEq/L)

PNSS 154

LRS 130

0.9% NaCl 154

D5 0.45% NaCL 77

D5 3% NaCl 513

Na

Deficit 256.03 mEq/L

Maintenance 3 x BW3 x 56= 168

Losses -

Total 424.03 meq/L

PNSS

__424.03 meq/L__ = 4.24 L 100 meq NaCl__4240mL = 176.7 cc/hr 24 hrs__176.7 cc/hr__ = 44.16 45gtts/min 4

Osmotic Demyelinating Syndrome

Osmotic Demyelination Syndrome• Cause:– rapid correction of hyponatremia

• Characterized by:– flaccid paralysis– dysarthria– dysphagia

• At risk:– prior cerebral anoxic injury– hypokalemia– malnutrition, especially secondary to alcoholism

Osmotic Demyelination Syndrome

• Diagnosis:– suspected clinically– confirmed by appropriate neuroimaging studies

• Treatment:– no specific treatment– supportive only

• Prevention:– hyponatremia should be corrected at a rate not in

excess of 10mmol/L/24hr or 0.5 mEq/L/Hr– diligently avoid hypernatremia