S3C21 - Fluids and Electrolytes Flashcards
Total Body Water
- total body water = 60% of weight
- of which 67% is ICF and 33% is ECF
- of the 33% ECF, 25% of it is in the IVF which means from the 60% TBW, 5% is IVF
Osmolality
- calculated and measured osmolality should be within 10 of each other
- ddx osmolar gap:
- decreased serum water content in setting of hyperlipidemia or hyperproteinemia
- other LMW substances in the serum:
- ethanol
- methanol
- isopropyl alcohol
- ehtylene glycol
- acteone
- ethyl ether
- paraldehyde
- lactate
- mannitol
Hyponatremia
defn: <135mEq/L
- caused by either water gain or Na loss or alteration in the distribution of body water
- <120 pt is likely to get symptoms: n/v, anorexia, muscle cramps, confusion, lethargy, seizures, coma
- seizures likely to occur is Na <113mEq/L
- symptoms are caused by the osmotic gradient the develops across the BBB and from water being drawn into the brain
- in acute severe hyponatremia the mortality rate is 50%
- chronic hyponatremia symptoms: ataxia, focal weakness, hemiparesis
**be aware of correcting too rapidly and causing central pontine myelinolysis
Urine Na in hyponatremia
- if renal system intact and working well then dilute urine should be made
- if urine [Na]<10mEq/L this indicates renal handling is intact
- if urine [Na] >20mEq/L this indicates intrinsic renal tubular damage or natriuretic response to hypervolemia
Hypertonic Hyponatremia: causes
Osmolality >295
- usually occurs from shift of water from ICF into ECF
- DDX:
- -hyperglycemia
- -mannitol
- -glycerol therapy
Often there is a volume deficit and fluids are necessary
Isotonic Hyponatremia: DDx
Osmolality 275-295
- also termed pseudohyponatremia because due to the high levels of plasma proteins/lipids this makes the lab report a hyponatremia where in fact the Na+ is normal
- do not need to treat the hyponatremia
DDX:
- hyperlipidemia
- hyperproteinemia (eg. multiple myeloma, waldenstrom macroglobulinemia)
p.119
Hypotonic Hyonatremia: Ddx
Omsolality <275
Hypovolemic:
- renal: diuretic use, salt-wasting nephropathy (RTA, CKD, interstitial nephritis), osmotic diuresis (glucose, urea, hyperproteinemia), mineralcorticoid deficiency (aldosterone)
- extra-renal: volume replacement with hypotonic fluids, GI loss (vomiting, diarrhea, fistula, suction), third-space loss (burn, pancreatitis, peritonitis), sweating - CF
Hypervolemic:
- Urinary Na >20mEq/L = renal failure
- inability to excrete free water
- Urinary Na <20mEq/L
- CHF (low-flow to kidneys stimulates ADH)
- Nephrotic syndrome
- cirrhosis - causes decreased protein production
- Tx: usually salt and water restriction, sometimes diuretics or dialysis
Euvolemic: tx - fluid restriction
- urine Na usually >20mEq/L
- SIADH
- Hypothyroid
- pain, stress, nausea, psychosis (stimulates ADH)
- Drugs: ADH, nicotine, sulfonylureas, morphine, barbiturates, NSAIDs, tylenol, carbamazepine, penothiazines, TCA, colchicine, clofibrate, cyclophosphamide, isoproterenol, tolbutamide, vincristine, MAOI
- water intoxication (psychogenic or lesion in thirst center)
- glucocorticoid deficiency (glucocorticoids are required to suppress ADH)
- PPV - ventilation
- porphyria
*
Diagnosis Of SIADH
6 criteria:
- hypotonic hyponatermia (low serum osmolality)
- innapropriately elevated urinary osmolality (>200mOsm/kg)
- elevated urinary Na (>20mEg/L)
- clinical euvolemia
- normal adrenal, renal, cardiac, hepatic, thyroid fxn
- correctable with water restriction
Causes of SIADH
CNS: tumor, trauma, infxn, CVA, SAH, GBS, DTs, MS
Pulmonary Dz: tumor, PNA, COPD, abscess, TB, CF
Carcinoma: lung, pacreas, thymoma, ovarian, lymphoma
Emergency treatment of hyponatremia
- usually do not have to address Na >120 in the ED
- Na <115 or symptomatic need treatment initiated immediately:
- get urine electrolytes
- if hypovolemic, calculate the Na deficit and replace with NS:
- total body [Na] deficit =
(desired plasma[Na] - actual plasma [Na]) xTBW - if severe (<120mEq/L), develops rapidly, or pt seizes/coma, 3% saline should be administered at 25-100mL/h
- rise in Na should be <0.5-1mEq/L per hour
- if pt seizing then Na can be raised by 1-2mEq/L per hour
- if chronic severe, only increase by max 0.5mEq/L/h (NMT 12mEq/L/d)
** symptoms may be irreversible!
Hypernatremia
Defn: Na > 150mEq/L
- most are related to severe volume loss
- Symptoms: irritability, increased muscle tone, seizures, coma, death, tremulous, ataxia, hyperreflexic, spastic
- if osmolality >350mOsm/kg mortality >50%
- if brain shrinkage occurs rapidly this can tear blood vessels and cause bleeds
DDx:
- Inadequate water intake (impaired thirst, unable to obtain water)
- Excessive sodium
- ioatrogenic administration (hypertonic saline)
- accidental/deliverate ingestion (salt water ingestion/drowning)
- mineralcorticoid/glucocorticoid excess
- primary aldosteronism, cushings
- peritoneal dialysis
- GI loss - vomiting, diearrhea, intestinal fistula
- renal loss
- central diabetes insipidus
- impaired renal fxn
- osmotic diuresis (hypercalcemia, decreased protein intake, sickel cell, multiple myeloma, amyloidosis, sarcoidosis, sjogren, nephrogenic DI)
- drugs/meds (EtoH, lithium, phenytoin, sulfonylureas, amphotericin, colchicine)
- skin loss -burns, sweating
-essential hypernatremia
Diabetes Insipidus
- failure of central of peripheral ADH response
- low urine osmolality (200-300) - excessive loss of hypotonic urine
- central - failure to excrete ADH
- distinguish b/w central and nephrogenic by taking the serum and urine osmolaritiy under water deprivation and what the response is to 5 units of vasopressin
- lack of response to fluid loss is diagnositc
- pts with central DI respond well to vasopressin (urine osmolarity >800mOsm/L), whereas nephrogenic DI does not respond
Causes:
- Central: neoplasm, pituitary surgery, trauma, granulomas
- Nephrogenic: familial, hypercalcemia, hypokalemia, renal dz, drugs, malnutrition, hematologic d/o
Hypernatremia Treatment
- volume repletion with NS or RL
- interestingly, in my hypernatremic states there is an overall body deficit of Na+
- once perfusion has been established, switch to 0.45% saline with goal of u/o 0.5cc/kg/h
- do not reduce Na by >10-15mEq/L/day
- each liter of water deficit results in serum[Na] rise of 3-5mEq/L
- if acute hypernatremia then can rapidly correct b/c idiogenic osmoles (taurine) have not had a chance to be present in the brain yet so less risk of cerebral edema
Hypokalemia
- normal value = 3.5-5mEq/L
- defn: <3.5mEq/L
- clinical manifestations occur at 2.5mEq/L
- tx:
- stable: can give 20mEq of K+ q30-60mins until desired dose achieved
- severe - give IV 10mEq increments over 30-60 mins
- NMT 40mEq to each litre of fluid and NMT 40mEq/h
- cardiac monitoring if infusion >20mEq/h
- 20mEq should raise serum K by 0.25mEq/L
Symptoms of Hypokalemia
- Cardio: HTN, orthostatic hypotension, worsening of dig tox, dysrhythmia,
- t-wave flattening, u waves, ST depression
- neuro: malaise, weak, fatigue, hyporeflexive, cramps, paresthesias, paralysis, rhabdo
- GI - ileus
- renal: nephrogenic DI, incrased ammonia
- endocrine - glucose intolerance
Causes of hypokalemia
- ECF to ICF shifts
- alkalosis, increased insulin, beta-adrenergics
- Decreased intake
- GI loss - n/v, NG suction, diarrhea (laxative, enema abuse), malabsorption, ureterosigmoidostomy, enteric fistula, villous adenoma
- renal loss: diuretics, primary/secondary aldosteronism, licorice, chew tobacco, RTA, osmotic diuresis
- drugs/toxins: carbenicillin, PCN, amphotericin B, l-dopa, lithium, thallium, theophylline, dopamine
- sweat loss
- other - hypomagnesemia, acute leukemia
Potassium rich foods
- baked potatos
- spinach
- lima beans
- dried prunes
- tomatoes
- bananas
Hyperkalemia
- defn: >5.5mEq/L
- clinical significance:
- dysrhythmias, v. fib, heart block, asystole
- other Sx: weakness, paresthesias, areflexia, ascending paralysis, GI sigs (nausea, vomiting, diarrhea)
ECG:
- 6.5-7.5: prolonged PR, tall peaked T, short QT
- 7.5-8: flattened P, WRS widening
- 10-12: QRS degradation into sinusoidal pattern
Hyperkalemia Treatment
- do ECG, if no changes on ECG then repeat test to make sure
- 5-6 : treat underlying cause
Emergency treatment:
- cardiac monitoring
- check for other lytes (Mg)
- 3 phases of treament:
- membrane stabilization
- intracellular shift of K
- remove/ excrete K from body
- NB - if calcium needs to be administered b/c of severity of hypokalemia, be wary of pts on digitalis b/c hypercalcemia will potentiate the toxic cardiac effects of digitalis (avoid giving Calcium to pts on dig)
Treatment:
- Calcium Gluconate 10% 10-20ml IV
or Calcium chloride 10% 5-10ml IV
**calcium chloride is 3x potent than calcium gluconate - NaHCO3 (Bicarb) 50-100mEq IV
- Insulin 5-10 units with 1-2 amps of D50W
- Ventolin 2.5mg neb
- Lasix 40mg IV
- hemodialysis
- 10% calcium chloride = 27.2 mg/ml
- 10% calcium gluconate = 9mg elemental calcium/mL
Calcium
- 1/3 of calcium is absorbed in small bowel
- 50% of intravascular calcium is protein bound, 45% is free active ions and it is these that are physiologically active
- 1g decrease in albumin results in a 0.8mg/dL decrease in total calcium with no change in ionized fraction
- alkalosis decreases ionized calcium with no decrease in total serum calcium
- acidosis increases the ionized calcium
Hypocalcemia - causes
- defn: <2mEq/L of ionized [Ca]
normal
- 2.10-2.50 mmol/L total
- 1.15-1.35 mmol/L ionized
- common causes: shock, sepsis, renal failure, pancreatitis, hypoparathyroidism, CKD
- pancreatitis - lipase is released which breaks down fat and th fatty acids then combine with Ca leading to overalll decrase in serum Ca
More causes:
- decreased absorption
- increased excretion - EtOH, CKD, diuretics
- Endocrine d/o - hypoparathyroidism, pseudohypoparathyroidism
- drugs - phosphates (Enemas/laxatives), phenytoin, gentamicin, tobramycin, cisplatin, heparin, protamine, glucagon, norepi, citrate, loop diuretics, glucocorticoids, magnesium sulfate, sodium nitroprusside
Hypocalcemia - Symptoms
- symptoms usually occur at <0.8mmol/L)
- paresthesias, increased DTR, irritable, positive chvostek or trousseau sign (chvostek is twitch of corner of mouth when tap over facial nerve) (trousseau is carpal sapsm with BP cuff up)
- General: weak, fatigue
- Neuro: tetany, chvostek, trousseau, paresthesias, confusion, hallucination, dementia, seizures, EPS
- Derm: hyperpigmentation, brittle hair, dry skin
- Cardio: heart failure, vasoconstriction
- Muscular: spasms, cramps, weakness
- Skeletal: osteodystrophy, rickets, osteomalacia
- Misc: denatl hypoplasia, cataracts, decreased insulin secreiton
Hypocalcemia - ECG
-prolonged QT
Hypocalcemia - Treatment
- if not severe, oral Calcium therapy +/- vit D
- 1mEq of elemental calcium = 20mg of calcium
- if symptomatic or severe (<0.65mmol/L):
- 10cc of 10% Calcium Chloride (or 10-30cc of 10% Ca-gluconate) over 10-20 mins followed by infusion of 10% CaCl2 at 0.02-0.08cc/kg/h
- use central line b/c calcium is a potenet vasoconstrictor
- be very cautious if pt on digitalis b/c calcium potentiates its toxicity
-during massive TFN if blood is given >1unit q5min then give 10cc of 10% CaCl2 every 4-6 units of blood
**check magnesium level, b/c hypocalcemia is difficult to correct of also hypomagnesemia present
Hypercalcemia - causes
- relatively common
- usually d/t hyperparathyroidism or malignancy
Causes:
- Malignancy: lung (SCC), breast, kidney, myeloma, leukemia
- endocrine: primary hyperparathyroidism, hyperthyroidism, pheochromocytoma, adrenal insufficiency, acromegaly
- drugs: hypervitamins D/A, thiazides, lithiu, hormonal therapy for breast ca.
- granulomatous dz: sarcoid, TB, histoplasmosis, coccidiodomycosis
- immobilizaiton
- miscellaneous - pagets of the bone, postrenal transplant, phosphate deplation syndrome
Hypercalcemia - Symptoms
-stones, bones (osteolysis), moans (psyc d/o), groans (constipation, pancreatitis, PUD)
General: malaise, weak, polydipsia, dehydration
Neuro: confusion, apathy, dpn, memory impairment, irritable, hallucinations, ataxia, hyporeflexive, hypotonia
Skeleteal: #, bone pain, deformities
Cardio: HTN, dysrhythmias, vascular calcifications, ECG abnormalities (QT shortening, coving of ST-T wave, widening of T wave, digitalis sensitivity)
GI: anorexia, wt loss, n/v, constipation, abdo pain, PUD, pancreatitis
Urologic: polyuria, nocturia, renal insufficiency, stones
Other - conjunctivitis, pruritus, keratopathy
Hypercalcemia ECG
- depressed ST segements
- wide T wave
- shortened ST segment
- shortened QT interval
- bradyarrhythmias, BBB, second-degree block or compete heart block, cardiac arrest
Hypercalcemia treatment
- initiate if symptomatic or <0.8mmol/L
- Goals: volume repletion with NS, decrease Ca+ moblizaiton from bone, correct underlying d/o
- check for K and Mg
- do not use lasix
- bisphosphonates (pamidronate 90mg IV over 24h)
- ? calcitonin for sever symptoms (4units/kg SC)
Magnesium sources
-dry beans, leafy greens, meat, cereals
Hypomagnesemia - causes
-common causes: EtOH, malnutrition, cirrhosis, pancreatitis, excessive GI losses (Diarrhea)
Redistribution: postparathyroidectomy, IV glucose, DKA correction, refeeding, acute pancreatitis
Extrarenal loss: NG suciton, lactation, profuse sweating, burns, sepsis, intestinal fistula, diarrha
Decreased intake: EtOHism, cirrhosis, bowel resection, malabsorption
Increased renal losses: ketoacidosis, drugs (loop diuretics, aminoglycosides, ampho B, vit D OD, EtOH, cisplatin), SIADH, hyperthyroid, hyperparathy., 1/2ary aldoseronism, K+ depletion, tubulointestinal renal dz
Hypomagnesemia symptoms
- neuro: tetany, weakness, cerebellar (ataxia, nystagmus, vertigo), confusion, Sz, apathy, irritability, paresthesias
- GI: dysphagia, anorexia, nausea
- Cardio: heart failure, dysrhythmias, hypotension
- Misc: hypokalemia, hypocalcemia, anemia
Hypomagnesemia treatment
- check K, Ca and PO4 as they are often also present
- orally: 6g MgSO4 per day (50mEq) oral
- or 2g IV MgSo4 over 2h and run the other 4-6g over the next 22h
Hypermagnesemia
- most common cause: renal disease (CKD) or ingestion or volume depletion or familial hypocalciuric hypercalcemia
- other causes: renal failure, laxatives, enemas, treatment of eclampsia, DKA, tumor lysis, rhabdo, hypothuroid, mineralocorticoid deficiency…
- symptoms: not usually symptomatic but may have nausea, somnolence, decreased DTR, respiratory depression, hypotension, heart block, cardiac arrest
- treatment:
- IV fluids and lasix if good renal fxn
- severe symptomatic hypermagnesemia can be treated with 5ml of 10% CaCl2 IV over 5 mins
-consider hypermagnesemia in pts with hyperkalemia or hypercalcemia
Hypochloremia
- normal values: 95-105mEq/L
- usually caused by excessive diuresis, vomitting, or NG drain
- chloride loss is usually through urine or GI losses resulting in volume contraction which leads to increased Na and HCO3 resorption which leads to an alkalosis
- low urinary Cl <10mEq/L in setting of met alkalosis implies chloride responisve alkalosis, if urinary levels of Cl are heigher >40mEq/L, the hypochloremia may be secondary to volume overload/dilution
- also, increased mineralocorticoid activity results in retention of HCO3 and Na at expense of H, K, and Cl loss
- treatment: if chloride-responsive metabolic alkalosis then give IV NS
Hyperchloremia
- usually caused by: excessive NS administration, volume depletion or metabolic acidosis with AG
- treat the underlying issue
Hypophosphatemia
- occurs rarely
- some conditions are related to phosphate depletion: hyperparathyroidism, malignancy, hypercalcemia, renal tubular defects, use of phosphate-binding antacids
- symptoms/signs: impaired platelet fxn, spherocytosis, weakness, tremors, paresthesias, decreased DTR, decreased mental status, anorexia, hyperventilation, impaired myocardial fxn
- tx: milk is excellent source of phophate
- or IV potassium phosphate 2.5-5mg/kg IV over 6h
Hyperphosphatemia
- most commonly seen in pts with renal dysfunction
- tx: restrict calcium phosphate intake
- if normal renal fxn then excretion can be increased with IV saline and acetazolamide
- can use oral phosphate binders to prevent absorption
- hemodialysis if severe
