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and he was discharged from the hospital 4days aer surgery. Amuscle biopsy performed 3months aer discharge
was consistent with Becker’s muscular dystrophy(BMD).
is case is very typical of what can occur during anesthesia in a patient with an undiagnosed primary myopathy. e anesthesiologist must be aware of the eects of
acute rhabdomyolysis and be prepared to treat severe
hyperkalemia.
2. Can other conditions cause peaked T waves on the
EKG similar to hyperkalemia? Prominent T waves can
be caused by many conditions other than hyperkalemia.
ese conditions include le ventricular hypertrophy,
pericarditis, early repolarization, and noninfarction
myocardial ischemia. e most signicant cause other
than hyperkalemia is an acute myocardial infarction
(MI). If the sudden appearance of prominent peaked
T waves occurs during surgery, is it hyperkalemia or an
FOLLOW- UP OFHYPOKALEMIA (CLINICAL
CASE#2)
Although the anesthesiologist expressed concern about
a potassium level of 3.0mmol/ L, the patient was asymptomatic. e patient wanted to proceed with the surgery.
Aer induction of anesthesia and tracheal intubation,
ventilation was controlled to avoid hyperventilation and
respiratory alkalosis. Plasmalyte was used for intraoperative uid administration because of its higher potassium
concentration (5 mEq/ L versus 3 mEq/ L for lactated
Ringer’s solution). Aserum potassium concentration was
measured every hour. At the conclusion of the 4- hour surgical procedure, the patient’s serum potassium concentration
was 3.3mmol/ L. e patient’s cardiac rhythm was stable
throughout the procedure.
is case is a very common preoperative presentation
of a patient with chronic hypertension who is receiving
thiazide diuretics. ese patients can have asymptomatic
hypokalemia, and aggressive treatment can cause more
problems than it will solve. For most cases, only careful cardiac monitoring and measurement of serial potassium levels
is necessary, as complications secondary to hypokalemia are
veryrare.
acute myocardial infarction? e critical observation
to make with respect to the QRS morphology is the
ST segment. ere may be J point elevation with
both conditions, but the ST segment remains concave
relative to the baseline with hyperkalemia and is
convex with an acute infarction. ere may also be a
greater likelihood of hypotension with an acute MI.
Preexisting conditions that predispose to hyperkalemia
such as myopathies can aid in the diagnosis. e
simplest diagnostic method is measurement of a plasma
potassium level. e acute hyperkalemia, however, may
be very transient, and the sample must be obtained
quickly for accurate diagnosis.
3. What are the therapeutic modalities for the treatment
of severe intraoperative hyperkalemia? e best therapy
for acute intraoperative hyperkalemia is administration
of calcium gluconate or calcium chloride. Calcium
gluconate is suitable for administration through a
peripheral intravenous line, whereas calcium chloride
should ideally be administered via a central venous line.
Calcium antagonizes potassium at the cell membrane
but does not directly aect the plasma potassium
concentration.
4. What is the lower limit of the serum potassium
CASE- BASED LEARNING DISCUSSION
concentration that is deemed acceptable for elective
surgery? Most of the body’s potassium is intracellular,
and the plasma potassium level is a poor indicator
1. Why are patients with muscular dystrophy susceptible
to hyperkalemia? Patients with Duchenne muscular
dystrophy have a complete absence of dystrophin.
Dystrophin is a large protein that confers structural
stability to the muscle membrane. Its presence also
inuences the expression of other proteins critical to
the function of muscle cell membranes. ere is also a
proliferation of extrajunctional acetylcholine receptors
(up- regulation). ese abnormalities increase the
susceptibility of the muscle membrane to damage by
succinylcholine and halogenated, inhaled anesthetics.
When exposed to these drugs, there can be a massive
release of intracellular contents, including potassium.
of total body potassium content. More importantly,
however, is the gradient between extracellular and
intracellular potassium. Patients can have a low plasma
potassium level and still have a normal extracellular
to intracellular potassium gradient. If the gradient is
normal, it is highly unlikely that the hypokalemia will
cause intraoperative complications. Hyperventilation,
however, should be avoided, as the resultant alkalosis
may shi potassium intracellularly and change the
transmembrane potassium gradient. How quickly
the hypokalemia developed provides an indirect
clue as to the potassium gradient. Apatient taking
long- term diuretics who has a plasma potassium level
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267
of 3.0mmol/ L most likely has a normal potassium
gradient and is of less concern than the patient who
develops hypokalemia over 24 to 48 hours. Apotassium
less than 3.0mmol/ L is of concern, and postponing
elective surgery would be reasonable.
5. What are the risks associated with rapid correction of
hypokalemia? If the transmembrane potassium gradient
is normal and potassium is administered, a relative
hyperkalemia can develop that causes serious ventricular
dysrhythmias. Any replacement of potassium during
surgery must proceed cautiously with continuous EKG
monitoring.
REFERENCES
1. Gumz ML, Rabinowitz L, Wingo CS. An integrated view of
potassium homeostasis. New England Journal of Medicine.
2015;373:60– 72.
2. Abriel H, Rougier J- S, Jalife J. Ion channel macromolecular complexes in cardiomyocytes:roles in sudden cardiac death. Circulation
Research. 2015;116:1971– 88.
3. Medford- Davis L, Raque Z. Derangements of potassium.
Emergency Medicine Clinics of North America. 2014;32:329– 47.
4. Unwin RJ, Lu FC, Shirley DG. Pathophysiology and management
of hypokalemia:a clinical perspective. Nature Reviews Nephrology.
2011;7:75– 84.
5. Roush GC, Kaur R, Ernst ME. Diuretics: a review and update.
Journal of Cardiovascular Pharmacology and erapeutics.
2014;9:5– 13.
6. Lazich I, Bakris GL. Prediction and management of hyperkalemia across the spectrum of chronic renal disease. Seminars in
Nephrology. 2014;34:333– 39.
7. Palmer BF. A physiologic- based approach to the evaluation of a
patient with hypokalemia. American Journal of Kidney Diseases.
2010;56:1184– 90.
8. Segura LG, Lorenz JD, Weingarten TN, et al. Anesthesia and
Duchenne or Becker muscular dystrophy:review of 117 anesthetic
exposures. Pediatric Anesthesia. 2013;23:855– 64.
9. Wong KC, Schafer PG, Schultz JR. Hypokalemia and anesthetic
implications. Anesthesia & Analgesia. 1993;77:1238– 60.
10. Shingarev R, Allon M. A physiologic- based approach to the treatment of acute hyperkalemia. American Journal of Kidney Diseases.
2010;56:578– 84.
HYPERKALEMIA/HYPOKALEMIA 267
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38.
HYPONATREMIA/ HYPERNATREMIA
Brian N.Egan
CLINICAL CASE#1
A 25- year- old, 80- kg man was accidentally shot in the right
leg with a shotgun while hunting with a friend in a rural
area. Transport of the victim from the accident site was difcult, and medical resources were limited. Fluid resuscitation was performed with 3 liters of 5% dextrose in water.
Upon arrival in the emergency department, he was con-
PATHOPHYSIOLOGY
ese two cases illustrate the extremes of dysnatremia.
Hyponatremia is the most common electrolyte disorder
and occurs in 15% to 30% of hospitalized patients. Even
mild hyponatremia is associated with increased mortality.
Hypernatremia is less common, but the clinical manifesta-
tions are oen subtle and can develop insidiously.
fused. His blood pressure was 90/ 55mmHg, and his heart
rate was 142 beats per minute. His hematocrit was 18%,
and his plasma sodium level was 116mmol/ L. Initial examination of his wound revealed extensive so tissue damage
to his right popliteal fossa and a lacerated popliteal artery
andvein.
MECHANISM
Plasma sodium concentration is tightly controlled between
135 and 142mmol/ L by a nely tuned osmoregulatory sys-
tem. Dysfunction of this system subjects cells to osmotic
stress. Cells swell in a hypotonic milieu and shrink in a
hypertonic environment. Since the brain is contained
CLINICAL CASE#2
within a rigid compartment (cranium) that permits only
limited volume expansion, brain cells are very sensitive to
A 32- year- old 60- kg woman with a history of central diabetes insipidus (CDI) was admitted the day of surgery for
elective resection of a pituitary stalk tumor. She routinely
took intranasal desmopressin (DDAVP) every 12 hours
and had routine measurement of her plasma sodium levels.
Her most recent sodium level was 136mmol/ L (5 weeks
prior to admission) and 140mmol/ L (2.5 weeks prior to
admission). e preoperative unit nurses noted that the
patient voided frequently. Since the operating room schedule was running late, an intravenous catheter was inserted
and the patient received 2 liters of lactated Ringer’s solution prior to induction of anesthesia. She walked to the
operating room. Upon arrival in the operating room, she
had a pleasant, relaxed disposition and conversed normally with the operating room personnel. Aer induction
of anesthesia and tracheal intubation, a lumbar drain and
arterial catheter were placed without diculty. e initial blood gas analysis revealed a plasma sodium level of
175mmol/ L.
osmotic stress. In most tissues, sodium and water pass freely
through capillary membranes into the interstitium via gaps
between endothelial cells. e osmotic gradient between
the cells and the plasma is, consequently, undisturbed. e
blood- brain barrier has tight endothelial junctions that slow
the passage of sodium. Water, however, can freely cross the
blood- brain barrier. Changes in plasma sodium concentra-
tions inuence the movement of water from the intravascu-
lar space to the brain, thereby eecting changes in brain cell
volume. Osmoreceptors (tonicity receptors) in the hypo-
thalamus control cell volume by altering thirst sensation
and vasopressin secretion. Sodium sensors in the anterior
wall of the third ventricle also inuence sodium processing.
Aplasma sodium less that 135mmol/ L inhibits thirst and
vasopressin secretion, thereby promoting renal water excre-
tion. As the plasma sodium concentration increases above
142 mmol/ L, vasopressin levels increase. Vasopressin is
synthesized in the hypothalamus and stored in the poste-
rior pituitary. Vasopressin increases water reabsorption by
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increasing aquaporin channels in the distal tubules and collecting ducts of the kidneys.
drugs, cancer chemotherapy, and angiotensin- converting
enzyme (ACE) inhibitors can also causeSIADH.
e rapidity with which hyponatremia develops inu-
HYPONATREMIA
Hyponatremia is the most common electrolyte disorder and
is associated with increased mortality. e causes of chronic
hyponatremia are many, but the common pathway is usually inappropriately high levels of circulating vasopressin
(Box38.1).1 e anesthesiologist is most likely to encounter
acute hyponatremia caused by rapid absorption of sodiumfree solutions such as occurs during transurethral resection
of the prostate, endoscopic surgery, or intravenous infusion
of large amounts of sodium- free water. Inappropriate secre-
ences outcome and response to therapy. Brain cells adapt
to chronic hyponatremia by excreting cytoplasmic organic
solutes (osmolytes: glutamate, taurine, and myoinositol).
Such an adaptation restores osmotic neutrality without
a change in cell water. Rapid correction of chronic hyponatremia, however, causes osmotic demyelination, because
the adapted cells do not have sucient time to restore the
osmolytes. e osmotic demyelination syndrome is caused
by a cascade of inammatory events that starts with massive
astrocyte death followed by cytokine release culminating in
demyelination.
2,3
tion of antidiuretic hormone (SIADH) can be secondary to
malignancies, central nervous system trauma, cystic brosis,
asthma, and positive pressure ventilation. Antidepressant
Risk
e risks of hyponatremia are dependent on the rapidity
with which it develops. Acute hyponatremia does not per-
BOX 38.1 CAUSES OFHYPONATREMIA
Syndrome ofInappropriate Antidiuretic Hormone Secretion
(SIADH)
Secretion by malignanttumors
mit the brain to adapt, and rapid movement of water into
brain cells will lead to cerebral edema. e primary risk to
patients with chronic hyponatremia is rapid correction that
leads to central nervous system dysfunction secondary to
osmotic demyelination.
Drugs
butyrophenones, carbamazepine, opiates, phenothiazines
Cystic brosis
Asthma
Cerebral salt- wasting syndrome
Subarachnoid hemorrhage
Traumatic braininjury
Glycine or sorbitol absorption
Transurethral resection of the prostate
Endoscopic surgery (hysteroscopy)
Adrenal insufciency
Hypothyroidism
Renal failure
Congestive heart failure
Assessment ofthe Patient
Signs and symptoms of hyponatremia are dependent on
the sodium level, the rapidity with which the hyponatremia develops, age of the patient, and presence of coexisting
diseases (Box 38.2).4 In elderly patients, even mild hyponatremia is associated with gait disturbances and an increased
risk of bone fracture. Patients with chronic, moderate
hyponatremia may benet from treatment with vasopressin
antagonists (vaptans). Vaptans act by rendering vasopressin
receptors unresponsive.
5
Case #1 describes a previously healthy young adult
who develops acute hypovolemia from traumatic blood
loss and resuscitation with a large volume of sodium- free
intravenous uid. His tachycardia and hypotension reect
the need for further volume resuscitation, and his change in
mental status (confusion) is a result of hyponatremia.
Considerations forAnesthesia
Any patient with a plasma sodium less than 130mmol/
L should be considered to be hyponatremic. e incidence of hyponatremia in patients undergoing major surgery is 6% to 12% and is associated with an increased risk
of perioperative mortality. Whether the hyponatremia or
HYPONATREMIA/HYPERNATREMIA 269
270
Na deficitNaNaTBW([ ][ ])
n
+++
()
=−×
p
n
+
()
p
+
()
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e simplest equation for calculation of a patient’s
BOX 38.2 SIGNS AND SYMPTOMS OFHYPONATREMIA
These are dependent on the sodium level, rapidity of develop-
ment, age, and coexisting diseases
Plasma Sodium:130– 135mmol/ L
May be asymptomatic
sodium decitis:
Unsteadiness
Plasma Sodium 120– 130mmol/ L
Fatigue
Malaise
Nausea
Gait disturbance
Plasma Sodium 115– 120mmol/ L
Headache
Restlessness
Lethargy
Plasma Sodium < 115mmol/ L
Seizures
Coma
Respiratoryarrest
TBW is the total body water (liters). TBW (liters) is
60% of lean body weight (kg ) in adult males and 50% of
lean body weight (kg ) in adult females.
is formula does not consider the infusate volume,
ongoing uid decits, sodium losses, or renal function. More
complex formulas attempt to consider these other variables.
e multiple variables and dynamic physiologic mechanisms that may inuence plasma sodium levels, however,
will aect the utility of any formula. Clinically, it is best to
calculate the sodium decit with the above formula, initiate
therapy, and frequently measure plasma sodium concentrations. Subsequent therapeutic adjustments can then be made
based on the eect of therapy and the clinical status of the
patient.
Over the course of the 5- hour surgery, the patient
received 4 units of packed red blood cells (RBCs) and
3 liters of 0.9% saline. In the postanesthesia care unit
(PACU), his hematocrit was 28% and his plasma sodium
was 124mmol/ L.
Follow- Up
Death
Surgical and trauma patients with acute hyponatremia usually have multiple factors that inuence plasma sodium lev-
the underlying disease process that causes the hyponatremia is responsible for the increased risk is unclear.5 Elderly
patients with chronic hyponatremia and comorbid diseases
are at the highest risk of postoperative complications secondary to hyponatremia.
els. Correction of sodium levels in this setting can generally
be achieved faster than correction of chronic hyponatremia
in elderly patient with comorbidities. Patients with chronic
hyponatremia are usually euvolemic; whereas, trauma victims may be hypovolemic, anemic, and may have neurologic
injuries that complicate therapy. Despite the best eorts to
Treatment
Correction of hyponatremia needs to be done gradually, as rapid overcorrection can lead to osmotic demyelination syndrome. Osmotic demyelination can cause cerebral
edema, seizures, quadriplegia, and death6 In patients with
chronic hyponatremia, correction of the plasma sodium
calculate uid and electrolyte decits, frequent measurement of plasma electrolytes is the best method to monitor
and adjust therapy.
During the rst 12 postoperative hours, his mentation
improved and his urine output increased. Two days aer
surgery, his plasma sodium was 132mmol/ L.
concentration should not exceed 6mmol/ L over 24 hours.
e rapidity of correction with acute hyponatremia has
not been studied, and recommendations are speculative.
Correction of acute hyponatremia by 2 to 5mmol/ L in total
should not, however, result in osmotic demyelination.
270 SECTION C. ELECTROLYTE DISTURBANCES
7,8
HYPERNATREMIA
Hypernatremia can cause severe morbidity and mortality
and may pose a greater risk than hyponatremia. e medical
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271
muscle weakness, lethargy, confusion, seizures, and cerebral
BOX 38.3 CAUSES OFHYPERNATREMIA
Diabetes Insipidus
Central (decreased vasopressin secretion)
Nephrogenic (impaired renal response to vasopressin)
Impaired WaterIntake
Mental disability
Physical inability
Infusion of hypertonicsaline
Osmotic diuresis
Loop diuretics
Hyperaldosteronism
Cushing’s syndrome
hemorrhage. Hypovolemia is common and can cause tachycardia and orthostatic hypotension.
e gradual onset of hypernatremia allows brain cells to
accumulate organic solutes and maintain normal cell volumes. ese patients may exhibit few, if any, symptoms of
hypernatremia. Measurement of plasma sodium levels may
be the only way to diagnose hypernatremia.
e patient from clinical case #2 was surprisingly free
of symptoms prior to surgery. It is likely that her use of
DDAVP was sporadic and she had adapted to a chronic
hypernatremicstate.
MANAGEMENT
Considerations forAnesthesia
literature reports 60% mortality a ssociated with plasma sodium
levels greater than 160mmol/ L.9 Development of hypernatremia ultimately results from an inability to take in enough free
water. Examples that the anesthesiologist routinely encounters
are individuals who are fasting, intubated, and cognitively or
physically impaired. Anesthesiologists also care for patients
with pituitary and renal diseases. All of these conditions limit
an individual’s ability to ingest free water and physiologically
respond to increasing sodium levels (Box38.3).
Risk
As with hyponatremia, the risks of hypernatremia are
dependent on the rapidity with which it develops. Acute
hypernatremia causes brain cells to shrink as water moves
across the cell membrane and into the plasma. e shrinking brain places strain and tension on cranial nerves and
intracranial blood vessels. Catastrophic intracranial hemorrhage and debilitating cranial nerve palsies may result.
Rapid development of hypernatremia has also been shown
to cause central pontine myelinosis, which is classically
associated with rapid correction of hyponatremia.10 e
main risk of chronic hypernatremia is rapid, aggressive correction that leads to cerebral edema with subsequent brain
herniation anddeath.
Assessment ofthe Patient
Most signs and symptoms of severe hypernatremia
(>160mmol/ L) are secondary to neurologic dysfunction
and will depend on how quickly the increase in plasma
sodium level occurred. Arapid increase in sodium can cause
ere are several immediate concerns for the patient
with hypernatremia. e rst is determining whether
the condition is acute or chronic. is will guide subsequent therapy to normalize the plasma sodium concentration. Second, hypernatremia causes cellular free water
to move into the plasma. e patient with chronic diabetes insipidus will void tremendous amounts of urine,
thereby causing signicant hypovolemia. e dehydration can lead to a smaller volume of distribution for some
medications. Hypernatremia is thought to increase the
patient’s minimum alveolar concentration (MAC) by
antagonizing the depression of action potentials caused
by anestheticdrugs.
Management of the patient in the operating room is a
dynamic process with respect to uid management. Many
formulas for calculation of electrolyte decit or excess are
based on static conditions. e best method for management of electrolyte disorders is an approximate calculation
for correction followed by frequent measurement of plasma
electrolytes as therapy progresses.
Treatment
Treatment will depend on the underlying cause of the
hypernatremia, the rapidity with which the hypernatremia developed, and the severity of neurologic dysfunction. Most causes of hypernatremia are secondary to
loss of water and dehydration (Box 38.3). In those cases,
rehydration is the primary goal. How quickly rehydration
occurs is inuenced by whether the hypernatremia is acute
or chronic.
HYPONATREMIA/HYPERNATREMIA 271
272
∆
[][]
Na Na
TBWV
ip
++
−
+
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An approximation of the eect of rehydration can be
made from the following formula:
found the patient to be doing very well without any neurologic symptoms. In this particular case, the hypernatremia
may have been acute or chronic. e endocrinologist and
+
[]
Na
=
p
neurosurgeon ultimately concluded that the diagnosis was
asymptomatic, acute hypernatremia.
[Na+]p=plasma sodium concentration (mmol/ L)
[Na+]i=infusate sodium concentration (mmol/ L)
TBW=total body water (liters)
CASE- BASED LEARNING DISCUSSION
V=volume of infusate (liters)
1. Should the sodium replacement of the young trauma
In general, correction of chronic hypernatremia can
proceed at a rate of 0.5mmol/ L/ hour with a target sodium
concentration of 145mmol/ L. Correction of acute hypernatremia can be accelerated to 1.0mmol/ L/ hour.
In this case, an arterial line was inserted aer the induction of anesthesia and the initial sodium concentration
was reported as 175 mmol/ L. Both the neurosurgeon and
the anesthesiologist were skeptical of this value, given the
patient’s normal mental status just before induction. e plan
included proceeding with the surgery, administering a small
victim have been more aggressive? It is not clear
how quickly sodium can be replaced in patients
with acute hyponatremia. e patient also needed
volume replacement and blood. Normal saline was the
only crystalloid administered and by the end of the
procedure the sodium had increased to 128mmol/ L
(calculated was 125mmol/ L). Aer adequate volume
replacement and with good renal function, excess water
was excreted and the sodium level normalized within
48 hours of surgery.
dose of DDAVP (2 mcg), and sending a sample to the central lab for verication. While waiting for the lab results, the
patient was hyperventilated to a PaCO2 of 35mmHg, 40 mL
of cerebrospinal uid was removed from the lumbar drain,
and surgery commenced. At the same time that the surgeon exposed the brain, the central lab reported the plasma
sodium to be 172mmol/ L. e surgeon noted that the brain
was extremely shrunken. Hyperventilation was stopped and
the PaCO2 was allowed to normalize over 30 minutes. Fiy
mL of preservative- free saline was infused through the lumbar drain, and an intravenous infusion of 0.2% NaCl was
started (1.0 liter total during surgery). At the conclusion of
tumor resection and just prior to closure of the cranium, the
surgeon noted an improvement in brain size and morphology. e patient emerged from anesthesia and was extubated
without diculty. In the recovery room, she was drowsy but
able to follow commands. Her cranial nerve responses were
2. Did patient #1 have signs of cerebral edema
preoperatively? Confusion and disorientation
in a trauma victim can have multiple causes (e.g.,
hypotension, closed head injury). Since there was no
history of head trauma, the most likely cause of his
confusion was early cerebral edema from hyponatremia.
Some immediate correction of the hyponatremia was
indicated.
3. Is rapid correction of chronic, severe hyponatremia
indicated? is situation is dierent from the acute
hyponatremia of the trauma patient, and correction of
chronic hyponatremia must be performed with caution.
Acorrection goal of 6mmol/ L during the rst 24
hours is unlikely to result in osmotic demyelination.
In general, undercorrection of chronic hyponatremia
carries less risk than overcorrection.
intact, and she moved all extremities spontaneously. Her
plasma sodium level in the PACU was 166mmol/ L. During
the rst night aer surgery, she experienced mild le- sided
facial weakness and weakness of her arms and legs. Abrain
MRI was negative, and her plasma sodium was normalized
over 72 hours. At discharge, the patient’s plasma sodium level
was 142mmol/ L, and her neurologic function was normal.
4. Why was the laboratory nding of hypernatremia
(175mmol/ L) in case #2 questioned? Aplasma
sodium concentration of 175mmol/ L is extremely
high and it is rather unlikely that the patient would be
asymptomatic.
5. Was the intraoperative uid management of case
#2 appropriate? e administration rate of free
Follow- Up
e patient did not suer any long- term morbidity from
this event. Afollow- up phone call, 1month aer discharge,
water infusion may have been too aggressive. e
transient neurologic symptoms the night of surgery
may have been secondary to early cerebral edema.
Calculation of the Δ Na+ that included 2 liters of
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273
preoperative lactated Ringer’s solution and 1.0 liters
of free water intraoperatively would yield a predicted
Na concentration of 169mmol/ L (actual was
166mmol/L). An acute reduction of this magnitude
is unlikely to cause cerebral edema. Fortunately, the
patient did not experience any long- term sequelae.
REFERENCES
1. Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia:expert panel recommendations. American Journal of Medicine. 2013;126:S1– S42.
2. Sterns RH. Disorders of plasma sodium:causes, consequences, and
correction. New England Journal of Medicine. 2015;372:55– 65.
3. Kengne FG, Nicaise C, Soupart A, etal. Astrocytes are an early target in osmotic demyelination syndrome. Journal of the American
Society of Nephrology. 2011;22:1834– 45.
4. Bagshaw SM, Townsend DR, McDermid RC. Disorders of sodium
and water balance in hospitalized patients. Canadian Journal of
Anesthesia. 2009;56:151– 16.
5. Berl T. Vasopressin antagonists. New England Journal of Medicine.
2015;372:2207– 16.
6. Sterns RH, Silver SM. Complications and management of hyponatremia. Current Opinion in Nephrology and Hypertension.
2016;25:114– 19.
7. Greenberg A, Verbalis JG, Amin AN, etal. Current treatment practice and outcomes: report of the hyponatremia registry. Kidney
International. 2015;88:167– 77.
8. Geoghegan P, Harrison AM, ongprayoon C, etal. Sodium correction practice and clinical outcomes in profound hyponatremia.
Mayo Clinic Proceedings. 2015;90:1348– 55.
9. Alshayeb HM, Showkat A, Babar F, etal. Severe hypernatremia
correction rate and mortality in hospitalized patients. American
Journal of the Medical Sciences. 2011;341:356– 60.
10. Androgue HJ, Madias NE. Hypernatremia. New England Journal of
Medicine. 2000;342:1493– 99.
HYPONATREMIA/HYPERNATREMIA 273
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39.
HYPOCALCEMIA/ HYPERCALCEMIA
Stephen F. Dierdorf
CLINICAL CASE#1
A 62- year- old female underwent a total thyroidectomy
for thyroid cancer. The thyroid gland was not enlarged,
and she was scheduled for same- day surgery. At admission to the same- day surgery unit, she felt well and
had no complaints. Vital signs:heart rate, 79 beats per
PATHOPHYSIOLOGY
Calcium has many physiologic functions, and calcium
abnormalities aect almost every system of the body.
Calcium- sensing receptors (CaSR), which are found in
most tissues and organs, play a vital role in maintaining
uid and electrolyte balance.
minute, blood pressure 108/ 71 mmHg, respiratory
rate, 14 breaths per minute, temperature 36.8 degrees
C.Induction and maintenance of anesthesia were uneventful, and surgery was completed in 3 hours. She was
observed in the recovery and same day surgery area for
6 hours after surgery. At the time of discharge there was
no evidence of postoperative bleeding. Eight hours after
discharge her husband admitted her to the emergency
room with complaints of weakness, perioral tingling and
numbness, and dyspnea.
MECHANISM
Calcium eects that are of special interest in the periopera-
tive period include cardiac eects (rhythm, contractility),
excitation- coupling of skeletal muscle, and synaptic trans-
mission at the neuromuscular junction.
Small amounts of calcium initiate the cardiac action potential by entering the cardiac cell through L- type voltage- gated
calcium channels. is early entry of calcium subsequently
triggers a massive release of calcium from the sarcoplasmic
reticulum (SR) through ryanodine receptors. Release of cal-
CLINICAL CASE#2
cium from the SR activates the actin and myosin interaction
with subsequent cardiac muscle contraction. Muscle relaxa-
A 54- year- old female was brought to the emergency
department (ED) by her husband for the recent development of confusion, weakness, nausea, and abdominal
pain. Her vital signs in the ED were heart rate 96 beats per
minute and irregular; blood pressure, 108/ 62mmHg; respiratory rate of 18 breaths per minute. Her past medical
history included poorly controlled chronic hypertension;
her internist recently added hydrochlorothiazide to her
enalapril in an attempt to gain better control. Five years
ago she passed two renal stones and fractured her right
forearm in afall.
Laboratory studies obtained in the ED were:hemoglobin 14.3 grams/ dL, hematocrit 45%; potassium 3.1mmol/
L; sodium 148mmol/ L; and calcium 4mmol/ L (16.1 mg/
dL) (1mmol/ L=4 mg/ dL).
tion occurs when myoplasmic calcium is actively transported
back into the SR. Some calcium is extruded from the myocardial cell during the relaxation phase.
1,2
e action of calcium at the skeletal muscle neuromuscular junction is just as important for muscle function as its
action in the myocardium. Vesicles in the presynaptic axon
terminal contain acetylcholine molecules. Depolarization
of the presynaptic membrane causes calcium channels to
open, and the inux of calcium releases the stored acetylcholine into the synaptic cle. Acetylcholine traverses the
synaptic cle, activates acetylcholine receptors on the postsynaptic muscle membrane and initiates muscle membrane
depolarization and subsequent muscle contraction.
e prominent role that calcium plays in controlling
and regulating many physiologic functions explains why
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275
changes in the concentration of calcium in the blood produces so much dysfunction. Ryanodine receptors (RyR)
are central to calcium transport. Mutations in the RyR are
responsible for a number of diseases, including malignant
hyperthermia (MH). ree isoforms of the RyR have been
identied: (1) RyR1 (heart), (2) RyR2 (skeletal muscle),
and (3)RyR3 (brain).
e normal serum concentration of calcium is 2.15 to
2.6mmol/ L (8.6 to 10.4 mg/ dL). Fiy- ve percent of calcium is bound to albumin, phosphate, and citrate, and 45%
is in the ionized form (1.17 to 1.33mmol/ L). e ionized
calcium level is more accurate in reecting the physiologic
status of calcium function. Serum ionized calcium levels
are closely regulated by the parathyroid gland via secretion of parathormone. Calcium- sensing receptors in the
parathyroid respond to changes in ionized calcium. As ionized calcium decreases, parathormone secretion increases.
Parathormone increases ionized calcium by its eects on
80%. e incidence of clinically signicant or potentially
signicant hypocalcemia is 20% to 30%. Routine measurement of parathyroid hormones levels, intraoperatively or
immediately aer surgery, can better predict which patients
are at risk for hypocalcemia.
4
e eect of hypocalcemia on the EKG is a prolongation of the Q- T interval due to a lengthening of the plateau phase of the cardiac action potential (Figure 39.1).
is increases calcium inow into the cell and predisposes to atrial and ventricular dysrhythmias (Box 39.1).5
Hypocalcemia reduces myocardial contractility, causing a
reduction in the cardiac output and hypotension. In rare
cases, hypocalcemia can cause acute cardiac failure.
Clinical manifestations of neuromuscular dysfunction caused by hypocalcemia include perioral numbness
and tingling, stridor, and dyspnea. Recurrent laryngeal
nerve injury, especially bilateral, can cause acute laryngeal
obstruction (vocal cord adduction).
bone, kidneys, and the gastrointestinal tract. Increases
in ionized calcium, by contrast, suppress parathormone
secretion.
Causes of hypercalcemia include hyperparathyroidism
(adenoma, hyperplasia, cancer), malignancy, vitamin D
toxicity, thyrotoxicosis, pheochromocytoma, rhabdomyolysis, and acute renal failure. Causes of hypocalcemia are
hypoparathyroidism, surgical excision of the parathyroid
glands during thyroidectomy, vitamin D deciency, acute
pancreatitis, and rapid infusion of citrate (blood products).
RISK OFHYPERCALCEMIA (CLINICAL CASE#2)
e two causes of hypercalcemia that are most likely to be
encountered in the surgical patient are primary hyperparathyroidism and hypercalcemia of malignancy. Primary hyperparathyroidism is caused by excessive parathyroid hormone
secretion by an adenoma, hyperplasia, or a malignancy of the
parathyroid gland. Most patients with primary hyperparathyroidism have chronic hypercalcemia and are relatively
asymptomatic. Chronic hypercalcemia does predispose to
RISK OFHYPOCALCEMIA (CLINICAL CASE#1)
Patients who develop hypocalcemia gradually can be surprisingly free of symptoms. Acute hypocalcemia, as may
occur aer thyroidectomy and inadvertent parathyroidectomy, is highly likely to provoke symptoms. e three most
common early complications aer total thyroidectomy are
hypocalcemia, recurrent laryngeal nerve injury, and hemorrhage.3 Based on calcium measurements aer thyroidectomy, the incidence of hypocalcemia varies from 5% to
nephrolithiasis and osteoporosis.6 Acute hypercalcemia may
occur in the asymptomatic patient when a drug that increases
calcium is administered to the patient. Symptoms of hypercalcemia occur when the serum calcium exceeds 3 mmol/ L
(12 mg/ dL). e patient from clinical case #2 developed a
further increase in calcium levels when hydrochlorothiazide
was added to her antihypertensive regimen.
Cancer can cause signicant hypercalcemia by several
mechanisms including the production of parathyroidhormone related protein (PTHrP) by the tumor. Squamous
Figure39.1 Long Q- T interval secondar y to hypocalcemia. SOURCE:From Crawford MH, DiMarco JP. Cardiology. NewYork, NY, Mosby, 2001:8, 4.7, with permission.
HYPOCALCEMIA/HYPERCALCEMIA 275
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